Nutrient chapter

Pantothenate (vitamin B5)

Vitamin precursor of the pantetheine moiety of coenzyme A.

116 recorded mechanisms · 35 availability situations · 7 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did.
Human thiamine transporter 2 / SLC19A3 → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated.
evidence-scope
Caco-2 and MDCK epithelial models
evidence_locator
Abstract
evidence_spans
[{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}]
experimental_model
Human transporter constructs in epithelial cell lines; uptake and surface targeting.
limitations
Tested cell models; clinical biotin-response mechanism remains unresolved.
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Human proteins in human and canine cell lines
plain_language
The name biotin-responsive disease does not make SLC19A3 a biotin carrier.
primary_references
[subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
tissue_or_cell_type
Caco-2 and MDCK epithelial models
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 294–307
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in epithelial cell lines; uptake and surface targeting. · source_derived_draft · unverified_draft
### b1-slc19a3-not-biotin-transporter Wild-type SLC19A3 did not confer detectable biotin uptake, whereas the SLC5A6 positive control did. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The name biotin-responsive disease does not make SLC19A3 a biotin carrier. organism: Human proteins in human and canine cell lines tissue_or_cell_type: Caco-2 and MDCK epithelial models experimental_model: Human transporter constructs in epithelial cell lines; uptake and surface targeting. limitations: Tested cell models; clinical biotin-response mechanism remains unresolved. cross_nutrient: Distinguishes thiamine transport from biotin transport; no shared-substrate mechanism demonstrated. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}] evidence_locator: Abstract evidence-scope: Caco-2 and MDCK epithelial models [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
Complete structured claim and evidence
Purified human PPCS, PPCDC and bifunctional CoA synthase reconstituted CoA synthesis from phosphopantothenate in vitro.
4-Phosphopantothenate → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Provides the B5-derived CoA partner required by PDH, OGDH, BCKDH and OADH; simultaneous B1/B5 depletion was not tested.
evidence
[{"paper_key": "daugherty-2002-coa", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Reconstituted human enzyme pathway.
limitations
Cross-pathway connection is biochemical integration, not a tested clinical supplementation interaction.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
Vitamin B5 supplies a separate carrier used after B1-dependent decarboxylation. The experiment starts with phosphorylated B5, so it does not test absorption or the first phosphorylation step.
primary_references
[daugherty-2002-coa] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant enzymes
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 731–743
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted human enzyme pathway. · source_derived_draft · unverified_draft
### b1-coa-b5-downstream-biosynthesis Purified human PPCS, PPCDC and bifunctional CoA synthase reconstituted CoA synthesis from phosphopantothenate in vitro. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin B5 supplies a separate carrier used after B1-dependent decarboxylation. The experiment starts with phosphorylated B5, so it does not test absorption or the first phosphorylation step. organism: Homo sapiens tissue_or_cell_type: Purified recombinant enzymes experimental_model: Reconstituted human enzyme pathway. limitations: Cross-pathway connection is biochemical integration, not a tested clinical supplementation interaction. evidence: [{"paper_key": "daugherty-2002-coa", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["abstract"], "locator": "Primary publication abstract", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: Provides the B5-derived CoA partner required by PDH, OGDH, BCKDH and OADH; simultaneous B1/B5 depletion was not tested. nutrient: Thiamine (vitamin B1) [daugherty-2002-coa] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Human RFK phosphorylates riboflavin to FMN using ATP, yielding ADP; this precedes FLAD1-mediated FAD synthesis.
Riboflavin kinase / RFK → Riboflavin (vitamin B2) source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract and product-bound structure
experimental_model
Human RFK structural and catalytic mechanism study
exposure
Purified RFK with flavin and adenine nucleotide ligands.
limitations
Reaction chemistry does not imply RFK controls every tissue flavin pool to the same extent.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Homo sapiens
plain_language
RFK performs the first activation step from riboflavin to FMN.
primary_references
[transport-rfk-2003] Ligand binding-induced conformational changes in riboflavin kinase: structural basis for the ordered mechanism. (2003). https://pubmed.ncbi.nlm.nih.gov/14580199/ DOI: 10.1021/bi035450t
tissue_or_cell_type
Purified protein
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 293–304
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human RFK structural and catalytic mechanism study · source_derived_draft · unverified_draft
### transport-rfk-phosphorylation Human RFK phosphorylates riboflavin to FMN using ATP, yielding ADP; this precedes FLAD1-mediated FAD synthesis. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: RFK performs the first activation step from riboflavin to FMN. organism: Homo sapiens tissue_or_cell_type: Purified protein experimental_model: Human RFK structural and catalytic mechanism study limitations: Reaction chemistry does not imply RFK controls every tissue flavin pool to the same extent. exposure: Purified RFK with flavin and adenine nucleotide ligands. evidence_location: Abstract and product-bound structure [transport-rfk-2003] Ligand binding-induced conformational changes in riboflavin kinase: structural basis for the ordered mechanism. (2003). https://pubmed.ncbi.nlm.nih.gov/14580199/ DOI: 10.1021/bi035450t
Complete structured claim and evidence
Human mitochondrial acetoacetyl-CoA thiolase ACAT1/T2, a homotetramer, uses coenzyme A to cleave acetoacetyl-CoA into two acetyl-CoA molecules.
Acetoacetyl-CoA → Acetyl-CoA source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified recombinant human ACAT1/T2 enzyme kinetics and crystal structures
limitations
Thiolase chemistry is reversible and shared with ketone metabolism. These experiments do not measure lysine-specific flux. ACAT1 here denotes acetyl-CoA acetyltransferase, not cholesterol acyltransferase SOAT1.
organism
Homo sapiens
plain_language
The four-carbon intermediate is split into two acetyl-CoA molecules.
primary_references
[haapalainen2007] Crystallographic and kinetic studies of human mitochondrial acetoacetyl-CoA thiolase: the importance of potassium and chloride ions for its structure and function (2007). https://pubmed.ncbi.nlm.nih.gov/17371050/ DOI: 10.1021/bi6026192
tissue_or_cell_type
Mitochondrial matrix enzyme; recombinant protein study
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 377–385
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human ACAT1/T2 enzyme kinetics and crystal structures · source_derived_draft · unverified_draft
### acat1-acetoacetyl-coa-thiolysis Human mitochondrial acetoacetyl-CoA thiolase ACAT1/T2, a homotetramer, uses coenzyme A to cleave acetoacetyl-CoA into two acetyl-CoA molecules. Plain language: The four-carbon intermediate is split into two acetyl-CoA molecules. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Mitochondrial matrix enzyme; recombinant protein study experimental_model: Purified recombinant human ACAT1/T2 enzyme kinetics and crystal structures limitations: Thiolase chemistry is reversible and shared with ketone metabolism. These experiments do not measure lysine-specific flux. ACAT1 here denotes acetyl-CoA acetyltransferase, not cholesterol acyltransferase SOAT1. [haapalainen2007] Crystallographic and kinetic studies of human mitochondrial acetoacetyl-CoA thiolase: the importance of potassium and chloride ions for its structure and function (2007). https://pubmed.ncbi.nlm.nih.gov/17371050/ DOI: 10.1021/bi6026192
Complete structured claim and evidence
Human phosphopantetheinyl transferase transfers a CoA-derived prosthetic group to ALDH1L2 Ser375.
Human 4-phosphopantetheinyl transferase / AASDHPPT → Human ALDH1L2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B5-derived CoA supplies phosphopantetheine; direct CoA handoff tested, dietary B5 link upstream.
experimental_model
Reconstitution and site-directed mutagenesis
exposure
Assay conditions described in the linked primary study.
limitations
Does not establish dietary B5 deficiency or repletion effects.
nutrient_topic
Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
organism
Homo sapiens
plain_language
A CoA-derived arm prepares the folate enzyme for catalysis.
primary_references
[strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008
tissue_or_cell_type
Cell-free
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1046–1057
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstitution and site-directed mutagenesis · source_derived_draft · unverified_draft
### aldh1l2-coa-arm Human phosphopantetheinyl transferase transfers a CoA-derived prosthetic group to ALDH1L2 Ser375. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A CoA-derived arm prepares the folate enzyme for catalysis. organism: Homo sapiens tissue_or_cell_type: Cell-free experimental_model: Reconstitution and site-directed mutagenesis limitations: Does not establish dietary B5 deficiency or repletion effects. exposure: Assay conditions described in the linked primary study. cross_nutrient: B5-derived CoA supplies phosphopantetheine; direct CoA handoff tested, dietary B5 link upstream. [strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008
Complete structured claim and evidence
Phosphopantetheinylation restored recombinant ALDH1L2 folate dehydrogenase activity with NADPH formation.
Human ALDH1L2 phosphopantetheinylated at Ser375 → 10-Formyltetrahydrofolate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
CoA maturation enables the folate-to-NADPH reaction.
experimental_model
Recombinant enzyme activation assay
exposure
Assay conditions described in the linked primary study.
limitations
Figure 5 used stable dideazafolate analogue rather than physiological folate.
nutrient_topic
Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
organism
Homo sapiens
plain_language
The installed arm enables oxidation of folate-bound carbon.
primary_references
[strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008
tissue_or_cell_type
Cell-free
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1059–1070
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant enzyme activation assay · source_derived_draft · unverified_draft
### aldh1l2-activation-folate-oxidation Phosphopantetheinylation restored recombinant ALDH1L2 folate dehydrogenase activity with NADPH formation. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The installed arm enables oxidation of folate-bound carbon. organism: Homo sapiens tissue_or_cell_type: Cell-free experimental_model: Recombinant enzyme activation assay limitations: Figure 5 used stable dideazafolate analogue rather than physiological folate. exposure: Assay conditions described in the linked primary study. cross_nutrient: CoA maturation enables the folate-to-NADPH reaction. [strickland-2011] Enzymatic properties of ALDH1L2, a mitochondrial 10-formyltetrahydrofolate dehydrogenase (2011). https://pubmed.ncbi.nlm.nih.gov/21238436/ DOI: 10.1016/j.cbi.2011.01.008
Complete structured claim and evidence
The human DLAT catalytic core contains a channel for the acetylated lipoyl group and CoA; substrate modeling positions CoA for acetyl-CoA formation.
Dihydrolipoyl acetyltransferase / DLAT → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B1-dependent E1 and B5-derived CoA participate in different sequential steps.
evidence
[{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Human DLAT cryo-EM; bacterial ligand poses used for modeling.
limitations
Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier.
primary_references
[jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357
tissue_or_cell_type
Purified catalytic core
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 690–702
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human DLAT cryo-EM; bacterial ligand poses used for modeling. · source_derived_draft · unverified_draft
### b1-pdh-dlat-coa-acetylation The human DLAT catalytic core contains a channel for the acetylated lipoyl group and CoA; substrate modeling positions CoA for acetyl-CoA formation. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: After B1 acts at E1, the E2 protein transfers the acetyl group onto CoA, a vitamin B5-derived carrier. organism: Homo sapiens tissue_or_cell_type: Purified catalytic core experimental_model: Human DLAT cryo-EM; bacterial ligand poses used for modeling. limitations: Ligand positions were modeled, not directly resolved in a human substrate-bound structure; no intake experiment. evidence: [{"paper_key": "jiang-2018-pdh-core", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-32"], "locator": "acetyl-accepting CoA", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1-dependent E1 and B5-derived CoA participate in different sequential steps. nutrient: Thiamine (vitamin B1) [jiang-2018-pdh-core] Atomic Structure of the E2 Inner Core of Human Pyruvate Dehydrogenase Complex (2018). https://pubmed.ncbi.nlm.nih.gov/29608861/ DOI: 10.1021/acs.biochem.8b00357
Complete structured claim and evidence
Human OGDH, lipoylated DLST and DLD assembled into an active complex coupling 2-oxoglutarate oxidation to NADH production in the CoA-containing assay.
2-Oxoglutarate dehydrogenase complex → Succinyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B1, B5-derived CoA, B2-derived FAD and niacin-related NAD act at different steps of one complex.
evidence
[{"paper_key": "nemeria-2014-ogdh", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-28"], "locator": "The reaction medium contained the following in 1.0 ml", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}]
experimental_model
Reconstituted human multienzyme assay.
limitations
NADH assay measures overall complex turnover, not every intermediate independently.
nutrient
Thiamine (vitamin B1) · Thiamine (vitamin B1)
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
B1-dependent E1 feeds a lipoyl/CoA transfer pathway, and E3 transfers the resulting reducing equivalents to NAD.
primary_references
[nemeria-2014-ogdh] Human 2-oxoglutarate dehydrogenase complex E1 component forms a thiamin-derived radical by aerobic oxidation of the enamine intermediate (2014). https://pubmed.ncbi.nlm.nih.gov/25210035/ DOI: 10.1074/jbc.m114.591073
tissue_or_cell_type
Purified enzyme complex
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 855–867
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted human multienzyme assay. · source_derived_draft · unverified_draft
### b1-ogdh-complex-couples-succinyl-nadh Human OGDH, lipoylated DLST and DLD assembled into an active complex coupling 2-oxoglutarate oxidation to NADH production in the CoA-containing assay. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1-dependent E1 feeds a lipoyl/CoA transfer pathway, and E3 transfers the resulting reducing equivalents to NAD. organism: Homo sapiens tissue_or_cell_type: Purified enzyme complex experimental_model: Reconstituted human multienzyme assay. limitations: NADH assay measures overall complex turnover, not every intermediate independently. evidence: [{"paper_key": "nemeria-2014-ogdh", "source_bundle": "artifacts/thiamine_metabolism_sources.json", "passage_ids": ["p-28"], "locator": "The reaction medium contained the following in 1.0 ml", "preservation": "Exact text retained in the source bundle; full source document retained when openly retrievable."}] cross_nutrient: B1, B5-derived CoA, B2-derived FAD and niacin-related NAD act at different steps of one complex. nutrient: Thiamine (vitamin B1) [nemeria-2014-ogdh] Human 2-oxoglutarate dehydrogenase complex E1 component forms a thiamin-derived radical by aerobic oxidation of the enamine intermediate (2014). https://pubmed.ncbi.nlm.nih.gov/25210035/ DOI: 10.1074/jbc.m114.591073
Complete structured claim and evidence
DHTKD1 with DLST and DLD supports oxidative decarboxylation of 2-oxoadipate to glutaryl-CoA, with NADH and carbon dioxide formation.
2-Oxoadipate → Glutaryl-CoA source_derived_draftungraded
Experimental context and source evidence
experimental_model
Recombinant human DHTKD1 and DLST; structural and biochemical assays; Two human patients; fibroblast isotope tracing and genetic complementation
limitations
DHTKD1 is the E1 component, not a stand-alone enzyme performing every complex reaction.
organism
Homo sapiens
plain_language
A three-enzyme complex converts the carbon skeleton into glutaryl-CoA.
primary_references
[bezerra2020] Crystal structure and interaction studies of human DHTKD1 provide insight into a mitochondrial megacomplex in lysine catabolism (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7340257/ DOI: 10.1107/S205225252000696X [danhauser2012] DHTKD1 mutations cause 2-aminoadipic and 2-oxoadipic aciduria (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3516599/ DOI: 10.1016/j.ajhg.2012.10.006
tissue_or_cell_type
Mitochondrial matrix
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 125–134
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human DHTKD1 and DLST; structural and biochemical assays; Two human patients; fibroblast isotope tracing and genetic complementation · source_derived_draft · unverified_draft
### oxoadipate-dehydrogenase-complex DHTKD1 with DLST and DLD supports oxidative decarboxylation of 2-oxoadipate to glutaryl-CoA, with NADH and carbon dioxide formation. Plain language: A three-enzyme complex converts the carbon skeleton into glutaryl-CoA. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Mitochondrial matrix experimental_model: Recombinant human DHTKD1 and DLST; structural and biochemical assays; Two human patients; fibroblast isotope tracing and genetic complementation limitations: DHTKD1 is the E1 component, not a stand-alone enzyme performing every complex reaction. [bezerra2020] Crystal structure and interaction studies of human DHTKD1 provide insight into a mitochondrial megacomplex in lysine catabolism (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7340257/ DOI: 10.1107/S205225252000696X [danhauser2012] DHTKD1 mutations cause 2-aminoadipic and 2-oxoadipic aciduria (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3516599/ DOI: 10.1016/j.ajhg.2012.10.006
Complete structured claim and evidence
FAD-containing human GCDH dehydrogenates glutaryl-CoA through glutaconyl-CoA and decarboxylates it to crotonyl-CoA.
Glutaryl-CoA → Crotonyl-CoA source_derived_draftungraded
Experimental context and source evidence
experimental_model
Human GCDH crystallography and substrate-mechanism analysis
limitations
The downstream shared ECHS1/HADH/ACAT1 reactions are separate records; these individual enzyme assays do not measure the full lysine-derived flux in a person.
organism
Homo sapiens
plain_language
GCDH shortens the lysine-derived carbon chain.
primary_references
[fu2004] Crystal Structures of Human Glutaryl-CoA Dehydrogenase with and without an Alternate Substrate: Structural Bases of Dehydrogenation and Decarboxylation Reactions (2004). https://pubs.acs.org/doi/10.1021/bi049290c DOI: 10.1021/bi049290c
tissue_or_cell_type
Mitochondrial matrix
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 136–144
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human GCDH crystallography and substrate-mechanism analysis · source_derived_draft · unverified_draft
### gcdh-crotonyl-coa FAD-containing human GCDH dehydrogenates glutaryl-CoA through glutaconyl-CoA and decarboxylates it to crotonyl-CoA. Plain language: GCDH shortens the lysine-derived carbon chain. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Mitochondrial matrix experimental_model: Human GCDH crystallography and substrate-mechanism analysis limitations: The downstream shared ECHS1/HADH/ACAT1 reactions are separate records; these individual enzyme assays do not measure the full lysine-derived flux in a person. [fu2004] Crystal Structures of Human Glutaryl-CoA Dehydrogenase with and without an Alternate Substrate: Structural Bases of Dehydrogenation and Decarboxylation Reactions (2004). https://pubs.acs.org/doi/10.1021/bi049290c DOI: 10.1021/bi049290c
Complete structured claim and evidence
EP300 transfers an acetyl group from acetyl-CoA to a protein lysine side chain.
EP300 → Protein-bound lysine residue source_derived_draftungraded
Experimental context and source evidence
experimental_model
Human p300 catalytic-domain structure and biochemical assays.
limitations
This reaction modifies lysine already in a protein. It does not show that extra oral lysine increases the reaction or improves a clinical outcome.
organism
Human
plain_language
Acetyl groups can be written onto lysines already present in proteins.
primary_references
[p300-2008] The structural basis of protein acetylation by the p300/CBP transcriptional coactivator (2008). https://pubmed.ncbi.nlm.nih.gov/18273021/ DOI: 10.1038/nature06546
tissue_or_cell_type
Not specified as a whole tissue; see experimental model.
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 527–535
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human p300 catalytic-domain structure and biochemical assays. · source_derived_draft · unverified_draft
### ep300-lysine-acetylation EP300 transfers an acetyl group from acetyl-CoA to a protein lysine side chain. Plain language: Acetyl groups can be written onto lysines already present in proteins. Condition category: normal organism: Human tissue_or_cell_type: Not specified as a whole tissue; see experimental model. experimental_model: Human p300 catalytic-domain structure and biochemical assays. limitations: This reaction modifies lysine already in a protein. It does not show that extra oral lysine increases the reaction or improves a clinical outcome. [p300-2008] The structural basis of protein acetylation by the p300/CBP transcriptional coactivator (2008). https://pubmed.ncbi.nlm.nih.gov/18273021/ DOI: 10.1038/nature06546
Complete structured claim and evidence
Human PCC supplies (S)-methylmalonyl-CoA by propionyl-CoA carboxylation upstream of the MCEE-MMUT sequence examined in fibroblast assays.
Human propionyl-CoA carboxylase / PCC → Propionyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Indexed primary abstract; Full text Methods 2.6 and Results 3.6; Figure 5
experimental_model
Human fibroblast PCC and coupled-pathway assays
exposure
Propionyl-CoA, ATP and bicarbonate in enzyme pathway
limitations
Pathway assignment combines human PCC characterization with coupled assays; it is not a simultaneous dietary biotin/B12 intervention.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Biotin-dependent PCC makes the precursor that must be rearranged before human MMUT can use B12 on it.
primary_references
[hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005 [heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
tissue_or_cell_type
Fibroblasts
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1159–1172
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human fibroblast PCC and coupled-pathway assays · source_derived_draft · unverified_draft
### pcc-carboxylation-upstream-b12 Human PCC supplies (S)-methylmalonyl-CoA by propionyl-CoA carboxylation upstream of the MCEE-MMUT sequence examined in fibroblast assays. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Biotin-dependent PCC makes the precursor that must be rearranged before human MMUT can use B12 on it. organism: Homo sapiens tissue_or_cell_type: Fibroblasts experimental_model: Human fibroblast PCC and coupled-pathway assays limitations: Pathway assignment combines human PCC characterization with coupled assays; it is not a simultaneous dietary biotin/B12 intervention. exposure: Propionyl-CoA, ATP and bicarbonate in enzyme pathway cross_nutrient: true evidence_location: Indexed primary abstract; Full text Methods 2.6 and Results 3.6; Figure 5 [hsia-1979-pcc] Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia. (1979). https://pubmed.ncbi.nlm.nih.gov/481943/ DOI: 10.1203/00006450-197906000-00005 [heuberger-2019-mcee] Genetic, structural, and functional analysis of pathogenic variations causing methylmalonyl-CoA epimerase deficiency. (2019). https://pubmed.ncbi.nlm.nih.gov/30682498/ DOI: 10.1016/j.bbadis.2019.01.021
Complete structured claim and evidence
Adenosylcobalamin-loaded human MMUT converts (R)-methylmalonyl-CoA to succinyl-CoA in the coupled enzyme assay.
Human methylmalonyl-CoA mutase / MMUT → (R)-Methylmalonyl-CoA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text Results; Figures 2-4; cofactor off-loading and MMUT activity Methods
experimental_model
Purified human proteins
exposure
AdoCbl-loaded MMUT and methylmalonyl-CoA; thiokinase-coupled readout
limitations
Product formation is a coupled assay; cellular net flux was not measured.
nutrient_topic
Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
organism
Homo sapiens
plain_language
Purified human MMUT used activated B12 to make succinyl-CoA from the matching methylmalonyl-CoA epimer.
primary_references
[mascarenhas-2023-nanoassembly] Architecture of the human G-protein-methylmalonyl-CoA mutase nanoassembly for B12 delivery and repair. (2023). https://pubmed.ncbi.nlm.nih.gov/37468522/ DOI: 10.1038/s41467-023-40077-4
tissue_or_cell_type
Purified protein assay
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1103–1115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human proteins · source_derived_draft · unverified_draft
### mmut-isomerizes-r-methylmalonyl-coa Adenosylcobalamin-loaded human MMUT converts (R)-methylmalonyl-CoA to succinyl-CoA in the coupled enzyme assay. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Purified human MMUT used activated B12 to make succinyl-CoA from the matching methylmalonyl-CoA epimer. organism: Homo sapiens tissue_or_cell_type: Purified protein assay experimental_model: Purified human proteins limitations: Product formation is a coupled assay; cellular net flux was not measured. exposure: AdoCbl-loaded MMUT and methylmalonyl-CoA; thiokinase-coupled readout cross_nutrient: false evidence_location: Full text Results; Figures 2-4; cofactor off-loading and MMUT activity Methods [mascarenhas-2023-nanoassembly] Architecture of the human G-protein-methylmalonyl-CoA mutase nanoassembly for B12 delivery and repair. (2023). https://pubmed.ncbi.nlm.nih.gov/37468522/ DOI: 10.1038/s41467-023-40077-4
Complete structured claim and evidence
Human ALAS2 uses PLP to condense glycine and succinyl-CoA into 5-aminolevulinate, releasing CoA and carbon dioxide.
Human erythroid aminolevulinate synthase 2 / ALAS2 → 5-Aminolevulinate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
B6 and glycine support the porphyrin precursor pathway upstream of iron insertion.
experimental_model
Purified recombinant human ALAS2; crystallography and kinetics
limitations
Iron insertion is a later ferrochelatase reaction, not an ALAS2 reaction.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
This B6-dependent step starts erythroid heme synthesis.
primary_references
[b6-alas2-2020] Human aminolevulinate synthase structure reveals a eukaryotic-specific autoinhibitory loop regulating substrate binding and product release (2020). https://www.nature.com/articles/s41467-020-16586-x DOI: 10.1038/s41467-020-16586-x
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 799–809
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human ALAS2; crystallography and kinetics · source_derived_draft · unverified_draft
### b6-met-alas2-ala Human ALAS2 uses PLP to condense glycine and succinyl-CoA into 5-aminolevulinate, releasing CoA and carbon dioxide. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This B6-dependent step starts erythroid heme synthesis. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human ALAS2; crystallography and kinetics limitations: Iron insertion is a later ferrochelatase reaction, not an ALAS2 reaction. cross_nutrient: B6 and glycine support the porphyrin precursor pathway upstream of iron insertion. [b6-alas2-2020] Human aminolevulinate synthase structure reveals a eukaryotic-specific autoinhibitory loop regulating substrate binding and product release (2020). https://www.nature.com/articles/s41467-020-16586-x DOI: 10.1038/s41467-020-16586-x
Complete structured claim and evidence
The human HADH homodimer reversibly oxidizes (S)-3-hydroxybutyryl-CoA to acetoacetyl-CoA while reducing NAD+ to NADH.
(S)-3-Hydroxybutyryl-CoA → Acetoacetyl-CoA source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified recombinant human HADH; substrate/product-cofactor crystal complexes
limitations
HADH is distinct from HADHA and HSD17B10. This shared reversible reaction supports the downstream route but does not quantify lysine-specific flux in people.
organism
Homo sapiens
plain_language
The four-carbon hydroxy intermediate is oxidized to a keto intermediate.
primary_references
[barycki2000] Sequestration of the active site by interdomain shifting. Crystallographic and spectroscopic evidence for distinct conformations of L-3-hydroxyacyl-CoA dehydrogenase (2000). https://pubmed.ncbi.nlm.nih.gov/10840044/ DOI: 10.1074/jbc.M004669200
tissue_or_cell_type
Mitochondrial short-chain hydroxyacyl-CoA metabolism; recombinant protein study
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 367–375
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human HADH; substrate/product-cofactor crystal complexes · source_derived_draft · unverified_draft
### hadh-hydroxybutyryl-coa-oxidation The human HADH homodimer reversibly oxidizes (S)-3-hydroxybutyryl-CoA to acetoacetyl-CoA while reducing NAD+ to NADH. Plain language: The four-carbon hydroxy intermediate is oxidized to a keto intermediate. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Mitochondrial short-chain hydroxyacyl-CoA metabolism; recombinant protein study experimental_model: Purified recombinant human HADH; substrate/product-cofactor crystal complexes limitations: HADH is distinct from HADHA and HSD17B10. This shared reversible reaction supports the downstream route but does not quantify lysine-specific flux in people. [barycki2000] Sequestration of the active site by interdomain shifting. Crystallographic and spectroscopic evidence for distinct conformations of L-3-hydroxyacyl-CoA dehydrogenase (2000). https://pubmed.ncbi.nlm.nih.gov/10840044/ DOI: 10.1074/jbc.M004669200
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of pantothenate.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries pantothenate into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 158–169
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-pantothenate Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of pantothenate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries pantothenate into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries biotin into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 171–182
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-biotin Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries biotin into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of lipoate.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular free lipoate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries lipoate into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 184–195
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-lipoate Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of lipoate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries lipoate into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Sodium-dependence kinetics of human SLC5A6-mediated pantothenate uptake supported a 2:1 sodium:pantothenate coupling ratio.
Sodium ion → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Sodium concentration-response of cloned human SMVT-mediated vitamin uptake.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 197–208
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-two-sodium-pantothenate Sodium-dependence kinetics of human SLC5A6-mediated pantothenate uptake supported a 2:1 sodium:pantothenate coupling ratio. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model. organism: Homo sapiens tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events. exposure: Sodium concentration-response of cloned human SMVT-mediated vitamin uptake. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Pantothenate evoked sodium-, concentration- and potential-dependent inward currents in Xenopus oocytes expressing human SLC5A6.
Pantothenate (vitamin B5) → Pantothenate-evoked SLC5A6 inward current source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Electrophysiology after human SMVT expression; pantothenate and extracellular sodium varied.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein); Xenopus laevis (expression host)
plain_language
Pantothenate transport through human SMVT moves net positive charge inward.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
Oocyte plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 210–221
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-pantothenate-current Pantothenate evoked sodium-, concentration- and potential-dependent inward currents in Xenopus oocytes expressing human SLC5A6. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pantothenate transport through human SMVT moves net positive charge inward. organism: Homo sapiens (protein); Xenopus laevis (expression host) tissue_or_cell_type: Oocyte plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Electrophysiology after human SMVT expression; pantothenate and extracellular sodium varied. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Functional full-length human SMVT-GFP localized to the apical membrane in the studied polarized intestinal epithelial cell lines.
Human sodium-dependent multivitamin transporter / SLC5A6 → Intestinal epithelial apical membrane source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines
exposure
Full-length human SMVT-GFP expression and polarized membrane imaging.
limitations
Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (transporter); expression-host species not specified in the retrieved abstract
plain_language
In the intestinal cell models, SMVT sits on the surface facing the intestinal contents.
primary_references
[b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008
tissue_or_cell_type
Polarized intestinal epithelial cell model
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 223–234
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines · source_derived_draft · unverified_draft
### b5-trans-epithelial-apical-targeting Functional full-length human SMVT-GFP localized to the apical membrane in the studied polarized intestinal epithelial cell lines. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: In the intestinal cell models, SMVT sits on the surface facing the intestinal contents. organism: Homo sapiens (transporter); expression-host species not specified in the retrieved abstract tissue_or_cell_type: Polarized intestinal epithelial cell model experimental_model: Functional human SMVT-GFP expression and imaging in polarized renal and intestinal epithelial cell lines limitations: Abstract-only; fluorescent fusion-protein localization in cell lines is not a measurement of net intestinal pantothenate absorption. The abstract does not name the intestinal cell line. exposure: Full-length human SMVT-GFP expression and polarized membrane imaging. cross_nutrient: true [b5-trans-targeting2009] Membrane targeting and intracellular trafficking of the human sodium-dependent multivitamin transporter in polarized epithelial cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19211916/ DOI: 10.1152/ajpcell.00396.2008
Complete structured claim and evidence
An inward sodium gradient drove transient pantothenate accumulation against its concentration gradient in voltage-clamped rabbit renal brush-border vesicles.
Sodium ion → Rabbit renal brush-border pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials
exposure
Inward NaCl gradient under voltage clamp; potassium, rubidium, lithium, ammonium and choline could not substitute for sodium.
limitations
Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Oryctolagus cuniculus
plain_language
Sodium provides energy for pantothenate uptake at the rabbit kidney brush border.
primary_references
[b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7
tissue_or_cell_type
Renal brush-border membrane vesicles
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 236–247
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials · source_derived_draft · unverified_draft
### b5-trans-renal-sodium-gradient An inward sodium gradient drove transient pantothenate accumulation against its concentration gradient in voltage-clamped rabbit renal brush-border vesicles. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium provides energy for pantothenate uptake at the rabbit kidney brush border. organism: Oryctolagus cuniculus tissue_or_cell_type: Renal brush-border membrane vesicles experimental_model: Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials limitations: Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold. exposure: Inward NaCl gradient under voltage clamp; potassium, rubidium, lithium, ammonium and choline could not substitute for sodium. cross_nutrient: true [b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7
Complete structured claim and evidence
An inside-negative membrane potential drove uphill pantothenate accumulation in rabbit renal brush-border vesicles when sodium was present even without a sodium concentration gradient.
Inside-negative potential in rabbit renal brush-border vesicles → Rabbit renal brush-border pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials
exposure
Inside-negative membrane potential imposed with sodium present but no transmembrane sodium gradient.
limitations
Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Oryctolagus cuniculus
plain_language
Electrical potential also helps power renal pantothenate uptake.
primary_references
[b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7
tissue_or_cell_type
Renal brush-border membrane vesicles
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 249–260
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials · source_derived_draft · unverified_draft
### b5-trans-renal-membrane-potential An inside-negative membrane potential drove uphill pantothenate accumulation in rabbit renal brush-border vesicles when sodium was present even without a sodium concentration gradient. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Electrical potential also helps power renal pantothenate uptake. organism: Oryctolagus cuniculus tissue_or_cell_type: Renal brush-border membrane vesicles experimental_model: Isolated rabbit renal brush-border membrane vesicles with controlled ion gradients and membrane potentials limitations: Rabbit isolated-membrane experiment; this predates molecular identification of SMVT and does not independently assign the effect to human SLC5A6 or establish a human renal clearance threshold. exposure: Inside-negative membrane potential imposed with sodium present but no transmembrane sodium gradient. cross_nutrient: true [b5-trans-renal1986] Pantothenate-sodium cotransport in renal brush-border membranes. (1986). https://pubmed.ncbi.nlm.nih.gov/3771539/ DOI: 10.1016/s0021-9258(18)66891-7
Complete structured claim and evidence
Dietary pantothenate level did not change mouse intestinal pantothenate uptake assayed at 5 micromolar, including comparisons involving pantothenate-deficient diets.
Pantothenate (vitamin B5) → Mouse intestinal pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays
exposure
High, normal and deficient pantothenate diets; uptake assayed at 5 micromolar. An antibiotic was needed to elicit severe deficiency; exact diet amounts and antibiotic are not reported in the abstract.
limitations
The abstract also describes a small late-deficiency increase in Vmax. A null result at 5 micromolar does not rule out all transport adaptation. Antibiotic use complicates attribution and does not quantify the human microbiome contribution.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Low dietary B5 did not cause a clear increase in intestinal B5 uptake at the tested concentration.
primary_references
[b5-trans-diet1989] Do dietary levels of pantothenic acid regulate its intestinal uptake in mice? (1989). https://pubmed.ncbi.nlm.nih.gov/2621490/ DOI: 10.1093/jn/119.12.1973
tissue_or_cell_type
Small intestine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 262–273
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays · source_derived_draft · unverified_draft
### b5-trans-dietary-deficiency-uptake Dietary pantothenate level did not change mouse intestinal pantothenate uptake assayed at 5 micromolar, including comparisons involving pantothenate-deficient diets. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low dietary B5 did not cause a clear increase in intestinal B5 uptake at the tested concentration. organism: Mus musculus tissue_or_cell_type: Small intestine experimental_model: Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays limitations: The abstract also describes a small late-deficiency increase in Vmax. A null result at 5 micromolar does not rule out all transport adaptation. Antibiotic use complicates attribution and does not quantify the human microbiome contribution. exposure: High, normal and deficient pantothenate diets; uptake assayed at 5 micromolar. An antibiotic was needed to elicit severe deficiency; exact diet amounts and antibiotic are not reported in the abstract. cross_nutrient: false [b5-trans-diet1989] Do dietary levels of pantothenic acid regulate its intestinal uptake in mice? (1989). https://pubmed.ncbi.nlm.nih.gov/2621490/ DOI: 10.1093/jn/119.12.1973
Complete structured claim and evidence
SLC5A6 knockdown analysis attributed 98.6% of total radiolabeled pantothenate uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells.
Human sodium-dependent multivitamin transporter / SLC5A6 → Human brain endothelial pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells
exposure
SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.
limitations
Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
SMVT supplied most measured pantothenate uptake in the human brain endothelial cell model.
primary_references
[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
tissue_or_cell_type
hCMEC/D3 cerebral microvascular endothelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 275–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft
### b5-trans-brain-pantothenate SLC5A6 knockdown analysis attributed 98.6% of total radiolabeled pantothenate uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT supplied most measured pantothenate uptake in the human brain endothelial cell model. organism: Homo sapiens tissue_or_cell_type: hCMEC/D3 cerebral microvascular endothelial cells experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue. exposure: SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
Complete structured claim and evidence
SLC5A6 knockdown analysis attributed 88.7% of total radiolabeled biotin uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells.
Human sodium-dependent multivitamin transporter / SLC5A6 → Human brain endothelial biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells
exposure
SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.
limitations
Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
SMVT supplied most measured biotin uptake in the human brain endothelial cell model.
primary_references
[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
tissue_or_cell_type
hCMEC/D3 cerebral microvascular endothelial cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft
### b5-trans-brain-biotin SLC5A6 knockdown analysis attributed 88.7% of total radiolabeled biotin uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT supplied most measured biotin uptake in the human brain endothelial cell model. organism: Homo sapiens tissue_or_cell_type: hCMEC/D3 cerebral microvascular endothelial cells experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Cellular luminal uptake is not itself a measurement of complete transendothelial delivery into brain tissue. Reported percentages apply to hCMEC/D3 under these assay conditions, not every human tissue. exposure: SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
Complete structured claim and evidence
The brain-microvessel study localized SLC5A6 preferentially to the luminal membrane of brain capillary endothelium.
Human sodium-dependent multivitamin transporter / SLC5A6 → Brain capillary luminal membrane source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells
exposure
Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses.
limitations
Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract
plain_language
Brain capillary SMVT is concentrated on the side facing the blood.
primary_references
[b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
tissue_or_cell_type
Brain capillary endothelium
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 301–312
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells · source_derived_draft · unverified_draft
### b5-trans-brain-luminal-localization The brain-microvessel study localized SLC5A6 preferentially to the luminal membrane of brain capillary endothelium. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Brain capillary SMVT is concentrated on the side facing the blood. organism: Homo sapiens and monkey microvessel preparations; localization sample allocation not detailed in abstract tissue_or_cell_type: Brain capillary endothelium experimental_model: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells limitations: Abstract does not resolve which species supplied every localization preparation. The result addresses blood-facing localization, not the unidentified abluminal export step. exposure: Antibody-free membrane-localization method, with human/monkey microvessel proteomics and human expression analyses. cross_nutrient: true [b5-trans-brain2015] Major involvement of Na(+) -dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25809983/ DOI: 10.1111/jnc.13092
Complete structured claim and evidence
Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls.
Intestine-specific Slc5a6-null mouse genotype → Mouse intestinal carrier-mediated biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake
exposure
Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays.
limitations
This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice.
primary_references
[b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012
tissue_or_cell_type
Intestinal epithelium
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 314–325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake · source_derived_draft · unverified_draft
### b5-trans-intestinal-knockout-biotin Intestine-specific Slc5a6 deletion completely inhibited the measured carrier-mediated intestinal biotin uptake component relative to littermate controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the shared vitamin transporter eliminated active intestinal biotin uptake in these mice. organism: Mus musculus tissue_or_cell_type: Intestinal epithelium experimental_model: Intestine-specific Slc5a6 conditional knockout mice compared with sex-matched littermates; in vivo and in vitro uptake limitations: This is shared transporter machinery impairment, not a dietary B5 depletion experiment. The abstract directly reports biotin uptake; no numerical pantothenate or lipoate absorption deficit is inferred. Passive uptake outside the measured carrier component is not excluded. exposure: Cre/lox-mediated intestinal Slc5a6 deletion; in vivo and in vitro biotin transport assays. cross_nutrient: true [b5-trans-intestinal-knockout2013] Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption. (2013). https://pubmed.ncbi.nlm.nih.gov/23104561/ DOI: 10.1152/ajpgi.00379.2012
Complete structured claim and evidence
Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells.
Biotin → Human SLC5A6 protein abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin
exposure
Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin.
limitations
Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Cells exposed to less biotin made more of the transporter also used by B5.
primary_references
[b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9
tissue_or_cell_type
JAr placental choriocarcinoma cells
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 327–338
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin · source_derived_draft · unverified_draft
### b5-trans-biotin-supply-smvt Across 25, 250 and 10000 pmol/L biotin culture conditions for three weeks, biotin availability correlated negatively with SMVT protein abundance in human JAr cells. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells exposed to less biotin made more of the transporter also used by B5. organism: Homo sapiens tissue_or_cell_type: JAr placental choriocarcinoma cells experimental_model: Human JAr choriocarcinoma cells cultured for three weeks with deficient, physiological or pharmacological biotin limitations: Tumor-derived placental cell model. The paper also measured biotin uptake and promoter activity, but a resulting change in pantothenate uptake or whole-placenta fetal delivery is not demonstrated by this abstract. exposure: Three weeks at 25 pmol/L deficient, 250 pmol/L physiological, or 10000 pmol/L pharmacological biotin. cross_nutrient: true [b5-trans-biotin-supply2004] Biotin supply affects rates of cell proliferation, biotinylation of carboxylases and histones, and expression of the gene encoding the sodium-dependent multivitamin transporter in JAr choriocarcinoma cells. (2004). https://pubmed.ncbi.nlm.nih.gov/14991266/ DOI: 10.1007/s00394-004-0435-9
Complete structured claim and evidence
Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.
Human SLC5A6 R94X truncated protein → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
limitations
Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R94X SMVT variant lost the uptake activity seen with the normal transporter.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r94x-biotin Expression of human SLC5A6 R94X failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R94X SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake.
Human SLC5A6 R123L protein variant → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake.
limitations
Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R123L SMVT variant lost the uptake activity seen with the normal transporter.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 353–364
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r123l-biotin Expression of human SLC5A6 R123L failed to induce biotin uptake above control in HuTu-80 and U87 cells, whereas wild-type SLC5A6 increased uptake. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R123L SMVT variant lost the uptake activity seen with the normal transporter. organism: Homo sapiens tissue_or_cell_type: HuTu-80 duodenal-derived epithelial and U87 brain-derived glioma cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Human transformed cell models expressing GFP-tagged constructs. Biotin is the measured substrate; impaired B5/lipoate transport is plausible through shared machinery but is not directly quantified here. Genetic dysfunction is not dietary B5 deficiency. exposure: Forty-eight hours after transfection; 5 nM [3H]biotin, pH 7.4, 37 degrees C, five-minute uptake. cross_nutrient: true [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
Human SLC5A6 R123L-GFP was predominantly retained in the endoplasmic reticulum; ER-marker colocalization supported this localization.
Human SLC5A6 R123L protein variant → Endoplasmic reticulum source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Live-cell confocal imaging 48 hours after transfection; hSMVT-GFP versus R123L-GFP and DsRed-ER.
limitations
Some mutant signal remained at the cell surface. Fluorescent-fusion localization does not prove zero residual activity or a dietary treatment response.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R123L transporter is largely trapped inside the cell instead of reaching its working surface.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 and U87 cells; ER-marker colocalization shown in HuTu-80
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 366–377
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r123l-er-retention Human SLC5A6 R123L-GFP was predominantly retained in the endoplasmic reticulum; ER-marker colocalization supported this localization. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R123L transporter is largely trapped inside the cell instead of reaching its working surface. organism: Homo sapiens tissue_or_cell_type: HuTu-80 and U87 cells; ER-marker colocalization shown in HuTu-80 experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Some mutant signal remained at the cell surface. Fluorescent-fusion localization does not prove zero residual activity or a dietary treatment response. exposure: Live-cell confocal imaging 48 hours after transfection; hSMVT-GFP versus R123L-GFP and DsRed-ER. cross_nutrient: false [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
The truncated SLC5A6 R94X-GFP construct was poorly expressed, with the detected signal localized in the cytoplasm of HuTu-80 and U87 cells.
Human SLC5A6 R94X truncated protein → Cytoplasm source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants
exposure
Live-cell confocal imaging of equal-DNA transfections under matched imaging settings.
limitations
Poor expression and localization were observed together; the experiment does not separately quantify synthesis, degradation and trafficking rates.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The R94X truncation produced little transporter and failed to show normal membrane localization.
primary_references
[b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
tissue_or_cell_type
HuTu-80 and U87 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 379–390
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants · source_derived_draft · unverified_draft
### b5-trans-r94x-cytoplasmic The truncated SLC5A6 R94X-GFP construct was poorly expressed, with the detected signal localized in the cytoplasm of HuTu-80 and U87 cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The R94X truncation produced little transporter and failed to show normal membrane localization. organism: Homo sapiens tissue_or_cell_type: HuTu-80 and U87 cells experimental_model: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants limitations: Poor expression and localization were observed together; the experiment does not separately quantify synthesis, degradation and trafficking rates. exposure: Live-cell confocal imaging of equal-DNA transfections under matched imaging settings. cross_nutrient: false [b5-trans-slc5a6-variants2017] Mutations in SLC5A6 associated with brain, immune, bone, and intestinal dysfunction in a young child. (2017). https://pubmed.ncbi.nlm.nih.gov/27904971/ DOI: 10.1007/s00439-016-1751-x
Complete structured claim and evidence
Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls.
Human SLC5A6 c.393+2T>C / p.Ser429Gly genotype → Human fibroblast biotin uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
experimental_model
Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis
exposure
The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts.
limitations
Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A patient with two SLC5A6 variants had a large defect in cellular biotin entry.
primary_references
[b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8
tissue_or_cell_type
Patient-derived fibroblasts
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis · source_derived_draft · unverified_draft
### b5-trans-patient-fibroblast-biotin Fibroblasts from the proband with SLC5A6 c.393+2T>C and p.Ser429Gly variants showed approximately 90% lower biotin uptake than controls. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A patient with two SLC5A6 variants had a large defect in cellular biotin entry. organism: Homo sapiens tissue_or_cell_type: Patient-derived fibroblasts experimental_model: Patient-derived fibroblasts in a human SLC5A6 family study; molecular and radiolabeled biotin uptake analysis limitations: Abstract-only transport extraction. This is one proband genotype, not an isolated p.Ser429Gly dose-response study; neither pantothenate uptake nor the relative contribution of individual supplements is quantified. exposure: The p.Ser429Gly allele supplied canonically spliced transcripts in the compound-heterozygous proband; uptake compared with control fibroblasts. cross_nutrient: true [b5-trans-neuropathy2024] Genome sequencing enables diagnosis and treatment of SLC5A6 neuropathy. (2024). https://pubmed.ncbi.nlm.nih.gov/38816490/ DOI: 10.1038/s41431-024-01641-8
Complete structured claim and evidence
Human SMVT cryo-EM complexes placed pantothenate, biotin and oxidized lipoate in substantially overlapping positions within one central substrate-binding pocket.
Human sodium-dependent multivitamin transporter / SLC5A6 → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures.
limitations
Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
B5, biotin and free lipoate use the same binding pocket in SMVT.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
Purified human SMVT; HEK293-derived expression system
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 405–416
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-shared-substrate-site Human SMVT cryo-EM complexes placed pantothenate, biotin and oxidized lipoate in substantially overlapping positions within one central substrate-binding pocket. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5, biotin and free lipoate use the same binding pocket in SMVT. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT; HEK293-derived expression system experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. These are separate ligand-bound complexes, not simultaneous occupancy. exposure: SMVTEM/NbALFA complexes incubated with 2 mM D-pantothenic acid, 4 mM biotin or 22 mM oxidized alpha-lipoic acid for separate structures. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
In the human SMVT–pantothenate structural model, the substrate carboxyl group interacts with backbone amino groups of Ser81/Ala84 and hydrogen-bonds to Tyr156.
Human sodium-dependent multivitamin transporter / SLC5A6 → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model.
limitations
Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
SMVT anchors the charged end of B5 through specific contacts in its binding pocket.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
Purified human SMVT ligand-binding pocket
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 418–429
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-pantothenate-carboxyl-recognition In the human SMVT–pantothenate structural model, the substrate carboxyl group interacts with backbone amino groups of Ser81/Ala84 and hydrogen-bonds to Tyr156. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT anchors the charged end of B5 through specific contacts in its binding pocket. organism: Homo sapiens tissue_or_cell_type: Purified human SMVT ligand-binding pocket experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: Engineered, purified transporter structure supports a binding mechanism; it does not establish nutritional competition severity in vivo. The structural construct has altered biotin transport kinetics relative to wild type. Atom-level interactions are structural-model interpretations; no specific dietary threshold follows. exposure: 3.7-angstrom cryo-EM pantothenate complex; molecular-dynamics support for the binding model. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay.
Pantothenate (vitamin B5) → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
limitations
In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
D-pantothenic acid competed with biotin uptake in the SMVT cell assay.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
HEK293T cells expressing human SMVT
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 431–442
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-pantothenate-inhibits-biotin D-pantothenic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 89.7 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: D-pantothenic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay.
Lipoic acid → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells
exposure
Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied.
limitations
In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay.
primary_references
[b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
tissue_or_cell_type
HEK293T cells expressing human SMVT
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 444–455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells · source_derived_draft · unverified_draft
### b5-trans-lipoate-inhibits-biotin Oxidized alpha-lipoic acid inhibited human SMVT-mediated radiolabeled biotin uptake with an IC50 of 9.1 micromolar in the 2026 HEK293T assay. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized alpha-lipoic acid competed with biotin uptake in the SMVT cell assay. organism: Homo sapiens tissue_or_cell_type: HEK293T cells expressing human SMVT experimental_model: Cryo-EM of engineered human SMVT with nanobody-assisted alignment; functional uptake assays in HEK293T cells limitations: In-vitro IC50 depends on tracer/substrate concentration and expression conditions; it is not a human supplement dose, affinity constant, or threshold for biotin deficiency. exposure: Biotin uptake assay: 5 micromolar unlabeled biotin plus [3H]biotin at a 300:1 molar ratio; 30 degrees C for ten minutes; inhibitor concentration varied. cross_nutrient: true [b5-trans-structure2026] Structural basis for multivitamin recognition and transport by human SMVT. (2026). https://pubmed.ncbi.nlm.nih.gov/42364996/ DOI: 10.1038/s41467-026-74948-3
Complete structured claim and evidence
Pantothenate at 10–1000 nmol/L reduced uptake of 475 pmol/L biotin by less than 12% in isolated human peripheral blood mononuclear cells.
Pantothenate (vitamin B5) → Human peripheral blood mononuclear cell biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays
exposure
10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin.
limitations
Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells.
primary_references
[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
tissue_or_cell_type
Isolated peripheral blood mononuclear cells
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 457–468
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft
### b5-trans-pbmc-small-competition Pantothenate at 10–1000 nmol/L reduced uptake of 475 pmol/L biotin by less than 12% in isolated human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: At the tested physiological concentrations, B5 only slightly reduced biotin entry into these blood cells. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: Cell-type-specific assay; the transporter was not molecularly identified as SLC5A6. This does not negate shared SMVT competition in other models and does not test high-dose supplementation. exposure: 10–1000 nmol/L pantothenic acid with 475 pmol/L [3H]biotin. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
Complete structured claim and evidence
Extracellular pantothenate did not significantly change biotin efflux from radiolabeled-biotin-loaded human peripheral blood mononuclear cells.
Pantothenate (vitamin B5) → Human peripheral blood mononuclear cell biotin efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays
exposure
[3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract.
limitations
P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Adding B5 outside these blood cells did not drive biotin back out.
primary_references
[b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
tissue_or_cell_type
Isolated peripheral blood mononuclear cells
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 470–481
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays · source_derived_draft · unverified_draft
### b5-trans-pbmc-efflux-null Extracellular pantothenate did not significantly change biotin efflux from radiolabeled-biotin-loaded human peripheral blood mononuclear cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding B5 outside these blood cells did not drive biotin back out. organism: Homo sapiens tissue_or_cell_type: Isolated peripheral blood mononuclear cells experimental_model: Isolated human peripheral blood mononuclear cells; radiolabeled biotin uptake and efflux assays limitations: P greater than 0.05 is a null result in this assay, not proof of no effect under every condition. The experiment does not identify a general B5 export transporter or SMVT-mediated exchange mechanism. exposure: [3H]biotin-loaded PBMC challenged with extracellular pantothenate; efflux-specific concentration not supplied in the abstract. cross_nutrient: true [b5-trans-pbmc1999] Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. (1999). https://pubmed.ncbi.nlm.nih.gov/15539319/ DOI: 10.1016/s0955-2863(99)00024-8
Complete structured claim and evidence
Human PANK3 catalyzes ATP-dependent conversion of pantothenate to 4′-phosphopantothenate.
Human pantothenate kinase 3 / PANK3 → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments
exposure
In-vitro biochemical exposure; concentrations not extracted.
limitations
Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
PANK3 starts vitamin B5 activation by adding phosphate.
primary_references
[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 483–494
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft
### b5-bio-pank3-phosphorylation Human PANK3 catalyzes ATP-dependent conversion of pantothenate to 4′-phosphopantothenate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PANK3 starts vitamin B5 activation by adding phosphate. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: true [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
Complete structured claim and evidence
Human PANK3 structures resolved Mg2+ in nucleotide-bound substrate and product complexes, directly connecting magnesium to the B5-phosphorylation machinery.
Mg2+ → Human pantothenate kinase 3 / PANK3 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments
exposure
In-vitro biochemical exposure; concentrations not extracted.
limitations
Structures used AMPPNP, ADP and related nucleotide complexes; ATP–Mg binding was assessed biochemically. This demonstrates catalytic-complex participation, not a dietary magnesium threshold or supplementation requirement.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Magnesium is part of the nucleotide complex used by PANK3.
primary_references
[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 496–507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft
### b5-bio-pank3-magnesium Human PANK3 structures resolved Mg2+ in nucleotide-bound substrate and product complexes, directly connecting magnesium to the B5-phosphorylation machinery. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium is part of the nucleotide complex used by PANK3. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Structures used AMPPNP, ADP and related nucleotide complexes; ATP–Mg binding was assessed biochemically. This demonstrates catalytic-complex participation, not a dietary magnesium threshold or supplementation requirement. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: true [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
Complete structured claim and evidence
Acetyl-CoA stabilizes an inactive human PANK3 dimer conformation, whereas ATP–Mg favors the active state; biochemical analyses showed coordinated switching of its two active sites.
Acetyl-CoA → Human pantothenate kinase 3 / PANK3 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments
exposure
In-vitro biochemical exposure; concentrations not extracted.
limitations
Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Accumulated acyl-CoA can slow the first step of new CoA production.
primary_references
[b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 509–520
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments · source_derived_draft · unverified_draft
### b5-bio-pank3-feedback Acetyl-CoA stabilizes an inactive human PANK3 dimer conformation, whereas ATP–Mg favors the active state; biochemical analyses showed coordinated switching of its two active sites. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Accumulated acyl-CoA can slow the first step of new CoA production. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human PANK3, crystallography and biochemical ligand-binding/heterodimer experiments limitations: Abstract-level structural and biochemical findings; no diet or Mg-repletion experiment. Substrate concentrations not established here. exposure: In-vitro biochemical exposure; concentrations not extracted. cross_nutrient: false [b5-bio-pank3allosteric] Allosteric Regulation of Mammalian Pantothenate Kinase. (2016). https://pubmed.ncbi.nlm.nih.gov/27555321/ DOI: 10.1074/jbc.m116.748061
Complete structured claim and evidence
Recombinant human PPCS ligated L-cysteine to 4′-phosphopantothenate in a nucleotide-dependent reaction forming 4′-phosphopantothenoylcysteine.
Phosphopantothenoylcysteine synthetase / PPCS → 4-Phosphopantothenate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
Coupled PPCS assay: 1.5 mM phosphopantothenate, 5 mM cysteine and 1 mM ATP or CTP; 2 mM MgCl2, pH 8.0, 37°C.
limitations
Human enzyme expressed in E. coli; assay substrate supply is not evidence that oral cysteine raises human CoA or that low blood cysteine gates B5 repletion.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Cysteine supplies the sulfur-containing portion of the developing CoA molecule.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 522–533
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-ppcs-ligation Recombinant human PPCS ligated L-cysteine to 4′-phosphopantothenate in a nucleotide-dependent reaction forming 4′-phosphopantothenoylcysteine. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cysteine supplies the sulfur-containing portion of the developing CoA molecule. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Human enzyme expressed in E. coli; assay substrate supply is not evidence that oral cysteine raises human CoA or that low blood cysteine gates B5 repletion. exposure: Coupled PPCS assay: 1.5 mM phosphopantothenate, 5 mM cysteine and 1 mM ATP or CTP; 2 mM MgCl2, pH 8.0, 37°C. cross_nutrient: true [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Under the reported coupled-assay conditions, human PPCS activated substrate with ATP about four times more efficiently than with CTP.
Phosphopantothenoylcysteine synthetase / PPCS → ATP source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
1 mM ATP versus 1 mM CTP, with 1.5 mM phosphopantothenate and 5 mM cysteine; 37°C.
limitations
Reported relative assay efficiency, not a universal kinetic constant; the paper contrasts the stronger CTP preference of E. coli PPCS.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Human PPCS favors ATP; bacterial nucleotide preferences should not be substituted for the human result.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 535–546
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-ppcs-atp-preference Under the reported coupled-assay conditions, human PPCS activated substrate with ATP about four times more efficiently than with CTP. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Human PPCS favors ATP; bacterial nucleotide preferences should not be substituted for the human result. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Reported relative assay efficiency, not a universal kinetic constant; the paper contrasts the stronger CTP preference of E. coli PPCS. exposure: 1 mM ATP versus 1 mM CTP, with 1.5 mM phosphopantothenate and 5 mM cysteine; 37°C. cross_nutrient: false [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Recombinant human PPCDC converted phosphopantothenoylcysteine to 4′-phosphopantetheine, verified by coupled enzyme assays and pathway reconstitution.
Phosphopantothenoylcysteine decarboxylase / PPCDC → 4′-Phosphopantothenoyl-L-cysteine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
Coupled assay used 50 micrograms/mL PPCDC with downstream COASY and 5 mM ATP; downstream ATP use is not assigned to PPCDC itself.
limitations
Coupled-assay confirmation and HPLC reconstitution; no dietary riboflavin depletion/repletion was tested.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
PPCDC removes the cysteine carboxyl group to produce the next CoA intermediate.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 548–559
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-ppcdc-decarboxylation Recombinant human PPCDC converted phosphopantothenoylcysteine to 4′-phosphopantetheine, verified by coupled enzyme assays and pathway reconstitution. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PPCDC removes the cysteine carboxyl group to produce the next CoA intermediate. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Coupled-assay confirmation and HPLC reconstitution; no dietary riboflavin depletion/repletion was tested. exposure: Coupled assay used 50 micrograms/mL PPCDC with downstream COASY and 5 mM ATP; downstream ATP use is not assigned to PPCDC itself. cross_nutrient: true [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Purified recombinant human PPCDC showed flavin-like absorbance maxima at 382 and 458 nm and approximately equimolar FMN association.
Phosphopantothenoylcysteine decarboxylase / PPCDC → Flavin mononucleotide source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
Purified human recombinant protein spectroscopy and cofactor characterization.
limitations
Direct enzyme-cofactor evidence; the study did not test dietary B2 deficiency, oral riboflavin rescue, or a universal FMN threshold. FMN origin from B2 is shared nutrient context, not a newly demonstrated dietary effect.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The CoA pathway contains a direct biochemical connection to the B2 cofactor FMN.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 561–572
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-ppcdc-fmn Purified recombinant human PPCDC showed flavin-like absorbance maxima at 382 and 458 nm and approximately equimolar FMN association. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The CoA pathway contains a direct biochemical connection to the B2 cofactor FMN. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Direct enzyme-cofactor evidence; the study did not test dietary B2 deficiency, oral riboflavin rescue, or a universal FMN threshold. FMN origin from B2 is shared nutrient context, not a newly demonstrated dietary effect. exposure: Purified human recombinant protein spectroscopy and cofactor characterization. cross_nutrient: true [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Human COASY phosphopantetheine adenylyltransferase activity used ATP and 4′-phosphopantetheine to form dephospho-CoA.
Coenzyme A synthase / COASY → 4′-Phosphopantetheine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
Forward PPAT assays: 5–500 micromolar phosphopantetheine and 5 mM ATP; 0.15–0.3 micrograms/mL recombinant COASY.
limitations
Direct biochemical reaction, distinct from the final phosphorylation; does not establish efficient entry of an oral intermediate into human cells.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
COASY adds the adenosine-containing portion of CoA.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 574–585
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-coasy-adenylylation Human COASY phosphopantetheine adenylyltransferase activity used ATP and 4′-phosphopantetheine to form dephospho-CoA. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: COASY adds the adenosine-containing portion of CoA. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Direct biochemical reaction, distinct from the final phosphorylation; does not establish efficient entry of an oral intermediate into human cells. exposure: Forward PPAT assays: 5–500 micromolar phosphopantetheine and 5 mM ATP; 0.15–0.3 micrograms/mL recombinant COASY. cross_nutrient: false [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Human COASY dephospho-CoA kinase activity phosphorylated dephospho-CoA to CoA using ATP; deleting the C-terminal domain retained PPAT but removed DPCK activity.
Coenzyme A synthase / COASY → 3′-Dephospho-coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution
exposure
DPCK assay: 5–100 micromolar dephospho-CoA, 1 mM ATP; coupled ADP readout and direct HPLC product analysis.
limitations
Recombinant enzyme and truncation studies define two distinct COASY activities; no whole-body nutritional threshold is measured.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The final COASY reaction completes CoA.
primary_references
[b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 587–598
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution · source_derived_draft · unverified_draft
### b5-bio-coasy-phosphorylation Human COASY dephospho-CoA kinase activity phosphorylated dephospho-CoA to CoA using ATP; deleting the C-terminal domain retained PPAT but removed DPCK activity. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The final COASY reaction completes CoA. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PPCS, PPCDC and COASY expressed in Escherichia coli; coupled enzyme assays and HPLC reconstitution limitations: Recombinant enzyme and truncation studies define two distinct COASY activities; no whole-body nutritional threshold is measured. exposure: DPCK assay: 5–100 micromolar dephospho-CoA, 1 mM ATP; coupled ADP readout and direct HPLC product analysis. cross_nutrient: false [b5-bio-daugherty2002] Complete reconstitution of the human coenzyme A biosynthetic pathway via comparative genomics. (2002). https://pubmed.ncbi.nlm.nih.gov/11923312/ DOI: 10.1074/jbc.m201708200
Complete structured claim and evidence
Acetyl-CoA inhibited purified human PANK2 competitively with ATP; PANK2 inhibition was submicromolar in the reported preparations.
Acetyl-CoA → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human PANK2 in 293T-cell lysates and purified enzyme assays
exposure
293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition.
limitations
The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
An existing CoA derivative feeds back to restrain PANK2.
primary_references
[b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 600–611
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft
### b5-bio-pank2-acetyl-inhibition Acetyl-CoA inhibited purified human PANK2 competitively with ATP; PANK2 inhibition was submicromolar in the reported preparations. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: An existing CoA derivative feeds back to restrain PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: The lysate IC50 is preparation-specific and is not a intracellular or dietary adequacy threshold. Purified-enzyme competition and lysate potency are separately identified. exposure: 293T-cell-lysate inhibition IC50 was 0.3 micromolar acetyl-CoA; purified-enzyme assays established ATP competition. cross_nutrient: false [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
Complete structured claim and evidence
Palmitoylcarnitine antagonized acetyl-CoA inhibition of human PANK2, providing a positive regulatory input in biochemical assays.
Palmitoyl-L-carnitine → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human PANK2 in 293T-cell lysates and purified enzyme assays
exposure
Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA.
limitations
Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A long-chain acylcarnitine can release the brake on PANK2.
primary_references
[b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 613–624
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft
### b5-bio-pank2-palmitoylcarnitine Palmitoylcarnitine antagonized acetyl-CoA inhibition of human PANK2, providing a positive regulatory input in biochemical assays. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A long-chain acylcarnitine can release the brake on PANK2. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: Acylcarnitine is a specific molecule; this does not show that free-carnitine supplements activate PANK2 in people. Intact-organism fatty-acid-demand interpretation was proposed. exposure: Human PANK2 in 293T lysates and purified-enzyme assays; indexed Fig. 1 used 0.2 micromolar acetyl-CoA. cross_nutrient: true [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
Complete structured claim and evidence
Free carnitine did not activate purified human PANK2 in the experiment shown in Fig. 4B.
L-Carnitine → Human pantothenate kinase 2 / PANK2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human PANK2 in 293T-cell lysates and purified enzyme assays
exposure
Primary Fig. 4B purified-enzyme assay; carnitine concentration range not extracted.
limitations
The same paper observed free-carnitine activation in lysate preparations at higher concentrations, so the purified-enzyme negative result must not be generalized to every lysate condition. Neither assay tests clinical carnitine supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The purified enzyme did not respond directly to free carnitine.
primary_references
[b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 626–637
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human PANK2 in 293T-cell lysates and purified enzyme assays · source_derived_draft · unverified_draft
### b5-bio-pank2-free-carnitine Free carnitine did not activate purified human PANK2 in the experiment shown in Fig. 4B. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The purified enzyme did not respond directly to free carnitine. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human PANK2 in 293T-cell lysates and purified enzyme assays limitations: The same paper observed free-carnitine activation in lysate preparations at higher concentrations, so the purified-enzyme negative result must not be generalized to every lysate condition. Neither assay tests clinical carnitine supplementation. exposure: Primary Fig. 4B purified-enzyme assay; carnitine concentration range not extracted. cross_nutrient: true [b5-bio-pank2reg] Activation of human mitochondrial pantothenate kinase 2 by palmitoylcarnitine. (2007). https://pubmed.ncbi.nlm.nih.gov/17242360/ DOI: 10.1073/pnas.0607621104
Complete structured claim and evidence
Human PANK2 was mitochondrial whereas mouse Pank2 localized to the cytosol in the comparative study.
Human pantothenate kinase 2 / PANK2 → Mouse pantothenate kinase 2 / Pank2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Comparative human and mouse PANK2 biochemistry and cellular localization
exposure
Comparative localization of human and mouse proteins; exact constructs/cell lines not extracted.
limitations
Localization difference must be retained when translating mouse knockout or rescue findings; this claim does not assign human PANK2 to a particular mitochondrial subcompartment.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens and Mus musculus
plain_language
The mouse Pank2 model differs from humans in where the enzyme resides.
primary_references
[b5-bio-pank2mouse] Localization and regulation of mouse pantothenate kinase 2. (2007). https://pubmed.ncbi.nlm.nih.gov/17825826/ DOI: 10.1016/j.febslet.2007.08.056
tissue_or_cell_type
Cellular subcellular-localization experiments
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 639–650
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative human and mouse PANK2 biochemistry and cellular localization · source_derived_draft · unverified_draft
### b5-bio-pank2-species-localization Human PANK2 was mitochondrial whereas mouse Pank2 localized to the cytosol in the comparative study. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mouse Pank2 model differs from humans in where the enzyme resides. organism: Homo sapiens and Mus musculus tissue_or_cell_type: Cellular subcellular-localization experiments experimental_model: Comparative human and mouse PANK2 biochemistry and cellular localization limitations: Localization difference must be retained when translating mouse knockout or rescue findings; this claim does not assign human PANK2 to a particular mitochondrial subcompartment. exposure: Comparative localization of human and mouse proteins; exact constructs/cell lines not extracted. cross_nutrient: false [b5-bio-pank2mouse] Localization and regulation of mouse pantothenate kinase 2. (2007). https://pubmed.ncbi.nlm.nih.gov/17825826/ DOI: 10.1016/j.febslet.2007.08.056
Complete structured claim and evidence
Biochemical testing found that human PANK4 lacks pantothenate kinase activity, unlike active PANK1–3 enzymes.
Human pantothenate kinase 4 / PANK4 → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons
exposure
Recombinant enzyme and catalytic-residue mutagenesis comparison; assay concentrations not extracted.
limitations
This is evidence about an enzyme paralogue, not loss of all cellular pantothenate phosphorylation. Other species PANK4 enzymes differ.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The protein named PANK4 is not another working B5 kinase in humans.
primary_references
[b5-bio-pank4pseudo] Human pantothenate kinase 4 is a pseudo-pantothenate kinase. (2019). https://pubmed.ncbi.nlm.nih.gov/30927326/ DOI: 10.1002/pro.3611
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 652–663
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons · source_derived_draft · unverified_draft
### b5-bio-pank4-pseudokinase Biochemical testing found that human PANK4 lacks pantothenate kinase activity, unlike active PANK1–3 enzymes. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein named PANK4 is not another working B5 kinase in humans. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human PANK4 biochemistry with evolutionary sequence and mutagenesis comparisons limitations: This is evidence about an enzyme paralogue, not loss of all cellular pantothenate phosphorylation. Other species PANK4 enzymes differ. exposure: Recombinant enzyme and catalytic-residue mutagenesis comparison; assay concentrations not extracted. cross_nutrient: false [b5-bio-pank4pseudo] Human pantothenate kinase 4 is a pseudo-pantothenate kinase. (2019). https://pubmed.ncbi.nlm.nih.gov/30927326/ DOI: 10.1002/pro.3611
Complete structured claim and evidence
Immunopurified full-length human PANK4 hydrolyzed phosphate from 4′-phosphopantetheine; D623A or D659A substitutions abolished the phosphatase activity.
Human pantothenate kinase 4 / PANK4 → 4′-Phosphopantetheine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays
exposure
Primary Fig. 4 biochemical assays with immunopurified Flag-PANK4, wild type versus D623A or D659A; substrate concentration not extracted.
limitations
Direct phosphatase assay. Divalent-metal participation was reported, but a particular nutritional mineral requirement is not assigned from these experiments.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
PANK4 can remove a phosphate from a CoA-building intermediate.
primary_references
[b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 665–676
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays · source_derived_draft · unverified_draft
### b5-bio-pank4-phosphatase Immunopurified full-length human PANK4 hydrolyzed phosphate from 4′-phosphopantetheine; D623A or D659A substitutions abolished the phosphatase activity. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PANK4 can remove a phosphate from a CoA-building intermediate. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays limitations: Direct phosphatase assay. Divalent-metal participation was reported, but a particular nutritional mineral requirement is not assigned from these experiments. exposure: Primary Fig. 4 biochemical assays with immunopurified Flag-PANK4, wild type versus D623A or D659A; substrate concentration not extracted. cross_nutrient: false [b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
Complete structured claim and evidence
Re-expression of active PANK4 in PANK4-knockout AKT p.E17K/+ MCF10A cells suppressed newly synthesized CoA, whereas phosphatase-inactive mutants did not reproduce the suppression.
Human pantothenate kinase 4 / PANK4 → Cellular de novo coenzyme A synthesis source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays
exposure
Wild-type versus D623A or D659A PANK4 re-expression; 3-hour carbon-13/nitrogen-15 vitamin-B5 labelling with growth factors.
limitations
Engineered cellular PI3K–AKT context; isotope concentration not verified. No claim that PANK4 controls every tissue or that dietary B5 produces the same response.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
PANK4 phosphatase activity can reduce new CoA production in cultured cells.
primary_references
[b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
tissue_or_cell_type
Human MCF10A mammary epithelial cells
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 678–689
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays · source_derived_draft · unverified_draft
### b5-bio-pank4-flux-suppression Re-expression of active PANK4 in PANK4-knockout AKT p.E17K/+ MCF10A cells suppressed newly synthesized CoA, whereas phosphatase-inactive mutants did not reproduce the suppression. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: PANK4 phosphatase activity can reduce new CoA production in cultured cells. organism: Homo sapiens tissue_or_cell_type: Human MCF10A mammary epithelial cells experimental_model: Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays limitations: Engineered cellular PI3K–AKT context; isotope concentration not verified. No claim that PANK4 controls every tissue or that dietary B5 produces the same response. exposure: Wild-type versus D623A or D659A PANK4 re-expression; 3-hour carbon-13/nitrogen-15 vitamin-B5 labelling with growth factors. cross_nutrient: false [b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
Complete structured claim and evidence
AKT phosphorylation of PANK4 relieved its suppression of de novo CoA synthesis in the study models.
AKT serine/threonine kinase family → Human pantothenate kinase 4 / PANK4 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays
exposure
PI3K–AKT signalling and PANK4 phosphorylation manipulations; no nutrient dosing trial.
limitations
Primary abstract with supporting cellular assays; mechanism is not a rationale for treating insulin signalling or increasing B5 intake.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Growth-factor signalling can ease the PANK4 brake on CoA production.
primary_references
[b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
tissue_or_cell_type
Human cultured-cell models
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 691–702
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays · source_derived_draft · unverified_draft
### b5-bio-akt-pank4-regulation AKT phosphorylation of PANK4 relieved its suppression of de novo CoA synthesis in the study models. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Growth-factor signalling can ease the PANK4 brake on CoA production. organism: Homo sapiens tissue_or_cell_type: Human cultured-cell models experimental_model: Human cultured-cell metabolomics and isotope tracing, PANK4 editing/re-expression and immunopurified human PANK4 phosphatase assays limitations: Primary abstract with supporting cellular assays; mechanism is not a rationale for treating insulin signalling or increasing B5 intake. exposure: PI3K–AKT signalling and PANK4 phosphorylation manipulations; no nutrient dosing trial. cross_nutrient: false [b5-bio-dibble2022] PI3K drives the de novo synthesis of coenzyme A from vitamin B5. (2022). https://pubmed.ncbi.nlm.nih.gov/35896750/ DOI: 10.1038/s41586-022-04984-8
Complete structured claim and evidence
Reconstituted human SLC25A42 transported CoA by counter-exchange and targeted mitochondria, supporting a route for mitochondrial CoA import.
Human mitochondrial coenzyme A transporter SLC25A42 → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Human SLC25A42 expressed in E. coli, purified and reconstituted into phospholipid vesicles, plus mitochondrial targeting experiments
exposure
Purified transporter proteoliposomes; substrate concentrations not extracted.
limitations
The experiment established exchange, not uniport. The proposed physiological import direction depends on metabolite gradients; the study does not establish that SLC25A42 is the sole importer.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Cells need transport machinery to supply the mitochondrial CoA compartment.
primary_references
[b5-bio-slc25a42] A novel member of solute carrier family 25 (SLC25A42) is a transporter of coenzyme A and adenosine 3',5'-diphosphate in human mitochondria. (2009). https://pubmed.ncbi.nlm.nih.gov/19429682/ DOI: 10.1074/jbc.m109.014118
tissue_or_cell_type
Reconstituted phospholipid vesicles and mitochondrial-targeting experiments
transport_effect
raises Counter-exchange transport that the record describes as a route for mitochondrial CoA import.
transport_pool
the mitochondrial matrix Counter-exchange transport that the record describes as a route for mitochondrial CoA import.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 704–715
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SLC25A42 expressed in E. coli, purified and reconstituted into phospholipid vesicles, plus mitochondrial targeting experiments · source_derived_draft · unverified_draft
### b5-bio-slc25a42-exchange Reconstituted human SLC25A42 transported CoA by counter-exchange and targeted mitochondria, supporting a route for mitochondrial CoA import. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells need transport machinery to supply the mitochondrial CoA compartment. organism: Homo sapiens tissue_or_cell_type: Reconstituted phospholipid vesicles and mitochondrial-targeting experiments experimental_model: Human SLC25A42 expressed in E. coli, purified and reconstituted into phospholipid vesicles, plus mitochondrial targeting experiments limitations: The experiment established exchange, not uniport. The proposed physiological import direction depends on metabolite gradients; the study does not establish that SLC25A42 is the sole importer. exposure: Purified transporter proteoliposomes; substrate concentrations not extracted. cross_nutrient: false [b5-bio-slc25a42] A novel member of solute carrier family 25 (SLC25A42) is a transporter of coenzyme A and adenosine 3',5'-diphosphate in human mitochondria. (2009). https://pubmed.ncbi.nlm.nih.gov/19429682/ DOI: 10.1074/jbc.m109.014118
Complete structured claim and evidence
The gene-discovery study identified recessive PANK2 defects as the cause of the studied inherited neurodegeneration with brain iron accumulation.
Human biallelic pathogenic PANK2 genotypes → Pantothenate kinase-associated neurodegeneration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Human recessive neurodegeneration gene-discovery study
exposure
Inherited recessive PANK2 defects; not a controlled vitamin-B5 depletion.
limitations
Primary gene-discovery abstract; proposed oxidative-stress mechanisms are not imported as proven consequences. No evidence here that pantothenate supplementation repairs the genetic lesion.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Inherited damage to a B5-using enzyme can cause disease even without low dietary B5.
primary_references
[b5-bio-pank2gene] A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11479594/ DOI: 10.1038/ng572
tissue_or_cell_type
Human neurological disease and genetic analysis
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 717–728
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recessive neurodegeneration gene-discovery study · source_derived_draft · unverified_draft
### b5-bio-pank2-genetic-disease The gene-discovery study identified recessive PANK2 defects as the cause of the studied inherited neurodegeneration with brain iron accumulation. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited damage to a B5-using enzyme can cause disease even without low dietary B5. organism: Homo sapiens tissue_or_cell_type: Human neurological disease and genetic analysis experimental_model: Human recessive neurodegeneration gene-discovery study limitations: Primary gene-discovery abstract; proposed oxidative-stress mechanisms are not imported as proven consequences. No evidence here that pantothenate supplementation repairs the genetic lesion. exposure: Inherited recessive PANK2 defects; not a controlled vitamin-B5 depletion. cross_nutrient: false [b5-bio-pank2gene] A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11479594/ DOI: 10.1038/ng572
Complete structured claim and evidence
The recombinant COASY DPCK domain carrying p.Arg499Cys did not produce a detectable CoA HPLC peak, whereas wild-type DPCK converted dephospho-CoA to CoA.
Human COASY p.Arg499Cys protein → 3′-Dephospho-coenzyme A source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies
exposure
HPLC assays with 1 microgram recombinant wild-type or p.Arg499Cys DPCK protein, ATP and dephospho-CoA; substrate concentrations not extracted.
limitations
Loss of detectable isolated-domain activity does not mean that every patient cell has no CoA. Wild-type and variant domains were recombinantly produced in bacteria.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
This COASY variant disabled the final reaction in the isolated-enzyme test.
primary_references
[b5-bio-coasy2014] Exome sequence reveals mutations in CoA synthase as a cause of neurodegeneration with brain iron accumulation. (2014). https://pubmed.ncbi.nlm.nih.gov/24360804/ DOI: 10.1016/j.ajhg.2013.11.008
tissue_or_cell_type
Purified recombinant protein; no intact tissue
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 730–741
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies · source_derived_draft · unverified_draft
### b5-bio-coasy-r499c-activity The recombinant COASY DPCK domain carrying p.Arg499Cys did not produce a detectable CoA HPLC peak, whereas wild-type DPCK converted dephospho-CoA to CoA. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: This COASY variant disabled the final reaction in the isolated-enzyme test. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies limitations: Loss of detectable isolated-domain activity does not mean that every patient cell has no CoA. Wild-type and variant domains were recombinantly produced in bacteria. exposure: HPLC assays with 1 microgram recombinant wild-type or p.Arg499Cys DPCK protein, ATP and dephospho-CoA; substrate concentrations not extracted. cross_nutrient: false [b5-bio-coasy2014] Exome sequence reveals mutations in CoA synthase as a cause of neurodegeneration with brain iron accumulation. (2014). https://pubmed.ncbi.nlm.nih.gov/24360804/ DOI: 10.1016/j.ajhg.2013.11.008
Complete structured claim and evidence
Free-CoA levels in fibroblasts from the two COASY cases were not significantly different from the control in the reported HPLC analysis.
Human pathogenic COASY genotypes in the Dusi 2014 cases → Free coenzyme A in primary fibroblasts source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies
exposure
Two affected individuals versus one healthy-control fibroblast line; four independent experiments shown in Fig. 6.
limitations
Small cell-line comparison and an absence of statistical significance, not proof of equal CoA in all compartments or tissues. Acetyl-CoA was significantly lower in one case; total-CoA trends and free-CoA results must not be conflated.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A severe enzyme defect did not imply an absent whole-cell free-CoA pool in these fibroblasts.
primary_references
[b5-bio-coasy2014] Exome sequence reveals mutations in CoA synthase as a cause of neurodegeneration with brain iron accumulation. (2014). https://pubmed.ncbi.nlm.nih.gov/24360804/ DOI: 10.1016/j.ajhg.2013.11.008
tissue_or_cell_type
Human primary skin fibroblasts
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 743–754
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies · source_derived_draft · unverified_draft
### b5-bio-coasy-fibroblast-free-coa Free-CoA levels in fibroblasts from the two COASY cases were not significantly different from the control in the reported HPLC analysis. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A severe enzyme defect did not imply an absent whole-cell free-CoA pool in these fibroblasts. organism: Homo sapiens tissue_or_cell_type: Human primary skin fibroblasts experimental_model: Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies limitations: Small cell-line comparison and an absence of statistical significance, not proof of equal CoA in all compartments or tissues. Acetyl-CoA was significantly lower in one case; total-CoA trends and free-CoA results must not be conflated. exposure: Two affected individuals versus one healthy-control fibroblast line; four independent experiments shown in Fig. 6. cross_nutrient: false [b5-bio-coasy2014] Exome sequence reveals mutations in CoA synthase as a cause of neurodegeneration with brain iron accumulation. (2014). https://pubmed.ncbi.nlm.nih.gov/24360804/ DOI: 10.1016/j.ajhg.2013.11.008
Complete structured claim and evidence
The salvage study reported extracellular CoA hydrolysis by ectonucleotide pyrophosphatases to 4′-phosphopantetheine.
Ectonucleotide pyrophosphatase/phosphodiesterase family → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments
exposure
Exogenous CoA; dose and assay-specific species not given in the abstract.
limitations
Abstract-level biochemical finding. ENPP isoform is unspecified here; this is not evidence for intact oral CoA delivery to the human brain.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Eukaryotic experimental systems; abstract does not assign species to this reaction
plain_language
External CoA can be processed into a smaller CoA-building intermediate.
primary_references
[b5-bio-salvage2015] Extracellular 4'-phosphopantetheine is a source for intracellular coenzyme A synthesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26322826/ DOI: 10.1038/nchembio.1906
tissue_or_cell_type
Extracellular biochemical/cell-culture environment
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 756–767
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments · source_derived_draft · unverified_draft
### b5-bio-extracellular-coa-processing The salvage study reported extracellular CoA hydrolysis by ectonucleotide pyrophosphatases to 4′-phosphopantetheine. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: External CoA can be processed into a smaller CoA-building intermediate. organism: Eukaryotic experimental systems; abstract does not assign species to this reaction tissue_or_cell_type: Extracellular biochemical/cell-culture environment experimental_model: Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments limitations: Abstract-level biochemical finding. ENPP isoform is unspecified here; this is not evidence for intact oral CoA delivery to the human brain. exposure: Exogenous CoA; dose and assay-specific species not given in the abstract. cross_nutrient: false [b5-bio-salvage2015] Extracellular 4'-phosphopantetheine is a source for intracellular coenzyme A synthesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26322826/ DOI: 10.1038/nchembio.1906
Complete structured claim and evidence
The 2015 salvage paper interpreted its experiments as passive membrane entry of extracellular 4′-phosphopantetheine before conversion back to CoA.
4′-Phosphopantetheine → Cellular entry of extracellular 4′-phosphopantetheine source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
experimental_model
Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments
exposure
Extracellular 4′-phosphopantetheine/CoA exposure; concentrations not extracted.
limitations
Author mechanistic interpretation preserved as a hypothesis. Abstract-only extraction cannot exclude extracellular dephosphorylation/rephosphorylation or establish passive uptake in every tissue, serum stability, or blood–brain-barrier delivery.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Eukaryotic cell/organism models; assay-level species not specified in abstract
plain_language
The authors proposed direct entry of the intermediate; the transport route remains a separate question from downstream enzyme activity.
primary_references
[b5-bio-salvage2015] Extracellular 4'-phosphopantetheine is a source for intracellular coenzyme A synthesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26322826/ DOI: 10.1038/nchembio.1906
tissue_or_cell_type
Cell membrane and intracellular CoA synthesis
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 769–780
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments · source_derived_draft · unverified_draft
### b5-bio-phosphopantetheine-entry-proposal The 2015 salvage paper interpreted its experiments as passive membrane entry of extracellular 4′-phosphopantetheine before conversion back to CoA. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The authors proposed direct entry of the intermediate; the transport route remains a separate question from downstream enzyme activity. organism: Eukaryotic cell/organism models; assay-level species not specified in abstract tissue_or_cell_type: Cell membrane and intracellular CoA synthesis experimental_model: Biochemical extracellular-CoA hydrolysis and eukaryotic cell/organism salvage experiments limitations: Author mechanistic interpretation preserved as a hypothesis. Abstract-only extraction cannot exclude extracellular dephosphorylation/rephosphorylation or establish passive uptake in every tissue, serum stability, or blood–brain-barrier delivery. exposure: Extracellular 4′-phosphopantetheine/CoA exposure; concentrations not extracted. cross_nutrient: false [b5-bio-salvage2015] Extracellular 4'-phosphopantetheine is a source for intracellular coenzyme A synthesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26322826/ DOI: 10.1038/nchembio.1906
Complete structured claim and evidence
Oral 4′-phosphopantetheine corrected the complex I activity defect in globus-pallidus-enriched brain tissue from Pank2-null mice.
4′-Phosphopantetheine → Mitochondrial complex I activity in Pank2-mutant mouse brain source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
C57/BL6 Pank2-null mice, both sexes aged 3–6 months, with globus-pallidus-enriched brain dissection; human PKAN cell experiments
exposure
Oral 4′-phosphopantetheine in 10% sucrose for 14 days; efficacy regimen 5 micrograms/g body weight (5 mg/kg); both-sex Pank2-null C57/BL6 mice aged 3–6 months; Fig. 2E n=5 per genotype/treatment group.
limitations
Biochemical rescue in mice, not a human efficacy result or proof of intact blood–brain-barrier delivery. The tissue was GP-enriched, not purified GP. Loss of Pank2 is machinery impairment, not dietary B5 withdrawal.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
A downstream intermediate improved a mitochondrial enzyme measurement in this genetic mouse model.
primary_references
[b5-bio-salvage2019] 4'-Phosphopantetheine corrects CoA, iron, and dopamine metabolic defects in mammalian models of PKAN. (2019). https://pubmed.ncbi.nlm.nih.gov/31660701/ DOI: 10.15252/emmm.201910489
tissue_or_cell_type
Globus-pallidus-enriched brain region; crude dissection also included neighboring structures
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 782–793
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · C57/BL6 Pank2-null mice, both sexes aged 3–6 months, with globus-pallidus-enriched brain dissection; human PKAN cell experiments · source_derived_draft · unverified_draft
### b5-bio-pank2-model-complex-i-rescue Oral 4′-phosphopantetheine corrected the complex I activity defect in globus-pallidus-enriched brain tissue from Pank2-null mice. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A downstream intermediate improved a mitochondrial enzyme measurement in this genetic mouse model. organism: Mus musculus tissue_or_cell_type: Globus-pallidus-enriched brain region; crude dissection also included neighboring structures experimental_model: C57/BL6 Pank2-null mice, both sexes aged 3–6 months, with globus-pallidus-enriched brain dissection; human PKAN cell experiments limitations: Biochemical rescue in mice, not a human efficacy result or proof of intact blood–brain-barrier delivery. The tissue was GP-enriched, not purified GP. Loss of Pank2 is machinery impairment, not dietary B5 withdrawal. exposure: Oral 4′-phosphopantetheine in 10% sucrose for 14 days; efficacy regimen 5 micrograms/g body weight (5 mg/kg); both-sex Pank2-null C57/BL6 mice aged 3–6 months; Fig. 2E n=5 per genotype/treatment group. cross_nutrient: false [b5-bio-salvage2019] 4'-Phosphopantetheine corrects CoA, iron, and dopamine metabolic defects in mammalian models of PKAN. (2019). https://pubmed.ncbi.nlm.nih.gov/31660701/ DOI: 10.15252/emmm.201910489
Complete structured claim and evidence
Human AASDHPPT transfers the 4′-phosphopantetheine moiety of CoA to a conserved serine in the human FASN acyl-carrier domain.
Coenzyme A → Human FASN phosphopantetheinylated ACP domain source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Abstract, substrate-specificity result
experimental_model
Recombinant human phosphopantetheinyl transferase and FASN ACP substrate
exposure
In-vitro enzymatic transfer from CoA; no dietary intervention.
limitations
Abstract-limited extraction; catalytic activation is distinguished from measuring whole-cell fatty-acid flux. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
CoA supplies the movable chemical arm used by the fatty-acid synthase carrier domain.
primary_references
[b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
tissue_or_cell_type
Cytosolic FASN ACP domain
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 795–807
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human phosphopantetheinyl transferase and FASN ACP substrate · source_derived_draft · unverified_draft
### b5-met-aasdhppt-fasn Human AASDHPPT transfers the 4′-phosphopantetheine moiety of CoA to a conserved serine in the human FASN acyl-carrier domain. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: CoA supplies the movable chemical arm used by the fatty-acid synthase carrier domain. organism: Homo sapiens tissue_or_cell_type: Cytosolic FASN ACP domain experimental_model: Recombinant human phosphopantetheinyl transferase and FASN ACP substrate limitations: Abstract-limited extraction; catalytic activation is distinguished from measuring whole-cell fatty-acid flux. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: In-vitro enzymatic transfer from CoA; no dietary intervention. cross_nutrient: false evidence_location: Abstract, substrate-specificity result [b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
Complete structured claim and evidence
Human AASDHPPT transfers the CoA-derived 4′-phosphopantetheine group to a conserved serine in human mitochondrial ACP.
Coenzyme A → Human phosphopantetheinylated mitochondrial ACP source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Abstract, substrate-specificity result
experimental_model
Recombinant human transferase and mitochondrial ACP substrate
exposure
Enzymatic transfer from CoA; no dietary intervention.
limitations
The experiment establishes substrate competence, not the in-vivo location of the transfer reaction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The mitochondrial carrier protein also needs a chemical arm derived from CoA.
primary_references
[b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
tissue_or_cell_type
Mitochondrial ACP substrate; in-vitro reaction
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 809–821
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human transferase and mitochondrial ACP substrate · source_derived_draft · unverified_draft
### b5-met-aasdhppt-mtacp Human AASDHPPT transfers the CoA-derived 4′-phosphopantetheine group to a conserved serine in human mitochondrial ACP. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mitochondrial carrier protein also needs a chemical arm derived from CoA. organism: Homo sapiens tissue_or_cell_type: Mitochondrial ACP substrate; in-vitro reaction experimental_model: Recombinant human transferase and mitochondrial ACP substrate limitations: The experiment establishes substrate competence, not the in-vivo location of the transfer reaction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Enzymatic transfer from CoA; no dietary intervention. cross_nutrient: false evidence_location: Abstract, substrate-specificity result [b5-met-joshi2003] Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity. (2003). https://pubmed.ncbi.nlm.nih.gov/12815048/ DOI: 10.1074/jbc.m305459200
Complete structured claim and evidence
Mitochondrial ACP knockdown in HEK293T cells reduced the proportion of mitochondrial proteins recognized as lipoylated before later respiratory defects.
Human mitochondrial acyl carrier protein / NDUFAB1 → Mitochondrial protein lipoylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Abstract, earliest phenotypic changes; Fig. 2 caption
experimental_model
Mitochondrial ACP siRNA in HEK293T cells
exposure
ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown.
limitations
Antibody-based lipoylation readout; not a measurement of dietary lipoic acid or pantothenate shortage. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Loss of the mitochondrial carrier impaired attachment of the lipoate cofactor to proteins.
primary_references
[b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
tissue_or_cell_type
HEK293T mitochondrial proteins
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 823–835
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft
### b5-met-mtacp-lipoylation Mitochondrial ACP knockdown in HEK293T cells reduced the proportion of mitochondrial proteins recognized as lipoylated before later respiratory defects. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of the mitochondrial carrier impaired attachment of the lipoate cofactor to proteins. organism: Homo sapiens tissue_or_cell_type: HEK293T mitochondrial proteins experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Antibody-based lipoylation readout; not a measurement of dietary lipoic acid or pantothenate shortage. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown. cross_nutrient: true evidence_location: Abstract, earliest phenotypic changes; Fig. 2 caption [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
Complete structured claim and evidence
Mitochondrial ACP knockdown in HEK293T cells subsequently reduced respiratory complex I specific activity.
Human mitochondrial acyl carrier protein / NDUFAB1 → Mitochondrial respiratory complex I source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Abstract, later phenotypic changes
experimental_model
Mitochondrial ACP siRNA in HEK293T cells
exposure
ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown.
limitations
Temporal ordering alone does not separate all direct complex-I effects from secondary cellular injury; abstract-level extraction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The carrier-protein defect also impaired complex I function.
primary_references
[b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
tissue_or_cell_type
HEK293T mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 837–849
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft
### b5-met-mtacp-complex-i Mitochondrial ACP knockdown in HEK293T cells subsequently reduced respiratory complex I specific activity. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carrier-protein defect also impaired complex I function. organism: Homo sapiens tissue_or_cell_type: HEK293T mitochondria experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Temporal ordering alone does not separate all direct complex-I effects from secondary cellular injury; abstract-level extraction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown. cross_nutrient: false evidence_location: Abstract, later phenotypic changes [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
Complete structured claim and evidence
Adding lipoic acid to the culture medium did not reverse the protein-lipoylation defect caused by mitochondrial ACP knockdown in HEK293T cells.
Lipoic acid → Mitochondrial protein lipoylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Abstract, lipoic-acid supplementation result
experimental_model
Mitochondrial ACP siRNA in HEK293T cells
exposure
Lipoic-acid supplementation of ACP-knockdown cultures; concentration not extracted.
limitations
Lipoic acid offered some oxidative-damage protection, but that is a different endpoint; result is not a universal statement about every lipoylation disorder. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
External lipoic acid did not bypass this carrier-protein defect.
primary_references
[b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
tissue_or_cell_type
HEK293T cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 851–863
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mitochondrial ACP siRNA in HEK293T cells · source_derived_draft · unverified_draft
### b5-met-lipoate-nonrescue Adding lipoic acid to the culture medium did not reverse the protein-lipoylation defect caused by mitochondrial ACP knockdown in HEK293T cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: External lipoic acid did not bypass this carrier-protein defect. organism: Homo sapiens tissue_or_cell_type: HEK293T cells experimental_model: Mitochondrial ACP siRNA in HEK293T cells limitations: Lipoic acid offered some oxidative-damage protection, but that is a different endpoint; result is not a universal statement about every lipoylation disorder. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Lipoic-acid supplementation of ACP-knockdown cultures; concentration not extracted. cross_nutrient: true evidence_location: Abstract, lipoic-acid supplementation result [b5-met-acp2009] Down-regulation of mitochondrial acyl carrier protein in mammalian cells compromises protein lipoylation and respiratory complex I and results in cell death. (2009). https://pubmed.ncbi.nlm.nih.gov/19221180/ DOI: 10.1074/jbc.m806991200
Complete structured claim and evidence
Endogenous yeast Acp1 copurified with Nfs1, Isd11 and Isu1; reciprocal immunoprecipitation confirmed association with the Nfs1–Isd11 core.
Saccharomyces cerevisiae mitochondrial acyl carrier protein / Acp1 → Saccharomyces cerevisiae Nfs1–Isd11 complex source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Full text lines 73; Fig. 1B and Fig. 1 supplement 3
experimental_model
Tagged endogenous protein immunoprecipitation and blue-native PAGE
exposure
Functional endogenous tagged proteins, detergent-solubilized mitochondria.
limitations
Stable association does not by itself quantify sulfur transfer; the protein identities are yeast, not human. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Saccharomyces cerevisiae
plain_language
The mitochondrial carrier physically associates with the iron–sulfur assembly machinery.
primary_references
[b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
tissue_or_cell_type
Isolated mitochondria
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 865–877
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tagged endogenous protein immunoprecipitation and blue-native PAGE · source_derived_draft · unverified_draft
### b5-met-yeast-acp-isu-binding Endogenous yeast Acp1 copurified with Nfs1, Isd11 and Isu1; reciprocal immunoprecipitation confirmed association with the Nfs1–Isd11 core. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mitochondrial carrier physically associates with the iron–sulfur assembly machinery. organism: Saccharomyces cerevisiae tissue_or_cell_type: Isolated mitochondria experimental_model: Tagged endogenous protein immunoprecipitation and blue-native PAGE limitations: Stable association does not by itself quantify sulfur transfer; the protein identities are yeast, not human. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Functional endogenous tagged proteins, detergent-solubilized mitochondria. cross_nutrient: true evidence_location: Full text lines 73; Fig. 1B and Fig. 1 supplement 3 [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
Complete structured claim and evidence
Conditional Acp1 depletion in yeast reduced assembled Nfs1–Isd11 and left the remaining Nfs1 and Isd11 predominantly in insoluble aggregates.
Saccharomyces cerevisiae mitochondrial acyl carrier protein / Acp1 → Saccharomyces cerevisiae Nfs1–Isd11 complex source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text line 117; Fig. 3A–B
experimental_model
TetO7-ACP1 conditional depletion and mitochondrial fractionation
exposure
10 micrograms/mL doxycycline for 18 hours to suppress ACP1.
limitations
Loss of cysteine-desulfurase activity was a mechanistic inference from complex destabilization, not a direct rate claim in this record. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Saccharomyces cerevisiae
plain_language
Removing the carrier destabilized the sulfur-handling protein complex.
primary_references
[b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
tissue_or_cell_type
Mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 879–891
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · TetO7-ACP1 conditional depletion and mitochondrial fractionation · source_derived_draft · unverified_draft
### b5-met-yeast-acp-complex-stability Conditional Acp1 depletion in yeast reduced assembled Nfs1–Isd11 and left the remaining Nfs1 and Isd11 predominantly in insoluble aggregates. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the carrier destabilized the sulfur-handling protein complex. organism: Saccharomyces cerevisiae tissue_or_cell_type: Mitochondria experimental_model: TetO7-ACP1 conditional depletion and mitochondrial fractionation limitations: Loss of cysteine-desulfurase activity was a mechanistic inference from complex destabilization, not a direct rate claim in this record. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 10 micrograms/mL doxycycline for 18 hours to suppress ACP1. cross_nutrient: true evidence_location: Full text line 117; Fig. 3A–B [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
Complete structured claim and evidence
The yeast Acp1 S82A variant, which cannot carry phosphopantetheine at that site, only modestly restored Nfs1–Isd11 abundance in Acp1-depleted cells, unlike wild-type Acp1.
Saccharomyces cerevisiae Acp1 S82A variant → Saccharomyces cerevisiae Nfs1–Isd11 complex source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text line 151; Fig. 4A–B
experimental_model
Wild-type versus S82A rescue of conditional yeast ACP1 depletion
exposure
Plasmid expression; 18 hours of 10 micrograms/mL doxycycline suppression.
limitations
S82A retained viability and some aconitase rescue. The study did not directly prove identical folding of apo and holo carrier proteins. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Saccharomyces cerevisiae
plain_language
The protein without its CoA-derived arm retained some function, but failed to restore normal complex stability.
primary_references
[b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
tissue_or_cell_type
Mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 893–905
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type versus S82A rescue of conditional yeast ACP1 depletion · source_derived_draft · unverified_draft
### b5-met-yeast-acp-s82a-partial The yeast Acp1 S82A variant, which cannot carry phosphopantetheine at that site, only modestly restored Nfs1–Isd11 abundance in Acp1-depleted cells, unlike wild-type Acp1. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The protein without its CoA-derived arm retained some function, but failed to restore normal complex stability. organism: Saccharomyces cerevisiae tissue_or_cell_type: Mitochondria experimental_model: Wild-type versus S82A rescue of conditional yeast ACP1 depletion limitations: S82A retained viability and some aconitase rescue. The study did not directly prove identical folding of apo and holo carrier proteins. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Plasmid expression; 18 hours of 10 micrograms/mL doxycycline suppression. cross_nutrient: true evidence_location: Full text line 151; Fig. 4A–B [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
Complete structured claim and evidence
Yeast PPT2 deletion, preventing mitochondrial ACP phosphopantetheinylation, reduced aconitase activity; a lipoate-synthesis LIP5 deletion control retained normal activity.
Saccharomyces cerevisiae mitochondrial phosphopantetheinyl transferase / Ppt2 → Total cellular aconitase activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text line 181; Fig. 4C–E
experimental_model
Yeast PPT2-deletion and LIP5-deletion comparison
exposure
Genetic deletion of PPT2, compared with wild type and LIP5 deletion.
limitations
Aconitase activity is the measured endpoint. The separate sulfite-reductase result is retained in the source, without duplicating it as another claim. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Saccharomyces cerevisiae
plain_language
Failure to install the carrier arm affected an iron–sulfur enzyme beyond the lipoate pathway.
primary_references
[b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
tissue_or_cell_type
Whole-cell enzyme assay; mitochondrial aconitase
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 907–919
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Yeast PPT2-deletion and LIP5-deletion comparison · source_derived_draft · unverified_draft
### b5-met-yeast-ppt2-fe-s Yeast PPT2 deletion, preventing mitochondrial ACP phosphopantetheinylation, reduced aconitase activity; a lipoate-synthesis LIP5 deletion control retained normal activity. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Failure to install the carrier arm affected an iron–sulfur enzyme beyond the lipoate pathway. organism: Saccharomyces cerevisiae tissue_or_cell_type: Whole-cell enzyme assay; mitochondrial aconitase experimental_model: Yeast PPT2-deletion and LIP5-deletion comparison limitations: Aconitase activity is the measured endpoint. The separate sulfite-reductase result is retained in the source, without duplicating it as another claim. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Genetic deletion of PPT2, compared with wild type and LIP5 deletion. cross_nutrient: true evidence_location: Full text line 181; Fig. 4C–E [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
Complete structured claim and evidence
Ndufab1 siRNA in mouse C2C12 myoblasts reduced mitochondrial Nfs1, Isd11 and Iscu2 protein abundance.
Mouse mitochondrial acyl carrier protein / Ndufab1 → Mouse cysteine desulfurase / Nfs1 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text line 117; Fig. 3C
experimental_model
Pooled Ndufab1 siRNA versus scrambled control
exposure
Ndufab1-targeting siRNA; immunoblot of isolated mitochondria.
limitations
The mammalian intact Nfs1–Isd11 complex could not be resolved by the authors with BN-PAGE; the direct mammalian result is subunit abundance. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
The iron–sulfur machinery also became less stable after carrier depletion in mouse muscle cells.
primary_references
[b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
tissue_or_cell_type
C2C12 myoblast mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 921–933
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pooled Ndufab1 siRNA versus scrambled control · source_derived_draft · unverified_draft
### b5-met-mouse-acp-isu-stability Ndufab1 siRNA in mouse C2C12 myoblasts reduced mitochondrial Nfs1, Isd11 and Iscu2 protein abundance. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The iron–sulfur machinery also became less stable after carrier depletion in mouse muscle cells. organism: Mus musculus tissue_or_cell_type: C2C12 myoblast mitochondria experimental_model: Pooled Ndufab1 siRNA versus scrambled control limitations: The mammalian intact Nfs1–Isd11 complex could not be resolved by the authors with BN-PAGE; the direct mammalian result is subunit abundance. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Ndufab1-targeting siRNA; immunoblot of isolated mitochondria. cross_nutrient: true evidence_location: Full text line 117; Fig. 3C [b5-met-acp2016] The mitochondrial acyl carrier protein (ACP) coordinates mitochondrial fatty acid synthesis with iron sulfur cluster biogenesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27540631/ DOI: 10.7554/elife.17828
Complete structured claim and evidence
In the recombinant hybrid NFS1–ISD11–ACP structure, the phosphopantetheine-linked acyl group of E. coli ACP occupies the hydrophobic core of human ISD11.
Escherichia coli acylated phosphopantetheinyl-AcpP → Human ISD11 / LYRM4 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Abstract; primary Results: Identification of the ACP–Lipid–ISD11 Motif
experimental_model
Hybrid recombinant human NFS1–ISD11 plus native E. coli ACP; X-ray/EM structure
exposure
Coexpression and structural analysis; no nutrient restriction.
limitations
This is not an all-human ACP structure. The bound PLP and acyl-ACP show cofactor coexistence; dietary B6/B5 dependency or repletion was not tested. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens proteins; Escherichia coli ACP
plain_language
The CoA-derived carrier arm holds a fatty-acid chain that helps form the iron–sulfur complex interface.
primary_references
[b5-met-cory2017] Structure of human Fe-S assembly subcomplex reveals unexpected cysteine desulfurase architecture and acyl-ACP-ISD11 interactions. (2017). https://pubmed.ncbi.nlm.nih.gov/28634302/ DOI: 10.1073/pnas.1702849114
tissue_or_cell_type
Purified recombinant Fe–S assembly subcomplex
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 935–947
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hybrid recombinant human NFS1–ISD11 plus native E. coli ACP; X-ray/EM structure · source_derived_draft · unverified_draft
### b5-met-acyl-acp-isd11-interface In the recombinant hybrid NFS1–ISD11–ACP structure, the phosphopantetheine-linked acyl group of E. coli ACP occupies the hydrophobic core of human ISD11. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The CoA-derived carrier arm holds a fatty-acid chain that helps form the iron–sulfur complex interface. organism: Homo sapiens proteins; Escherichia coli ACP tissue_or_cell_type: Purified recombinant Fe–S assembly subcomplex experimental_model: Hybrid recombinant human NFS1–ISD11 plus native E. coli ACP; X-ray/EM structure limitations: This is not an all-human ACP structure. The bound PLP and acyl-ACP show cofactor coexistence; dietary B6/B5 dependency or repletion was not tested. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Coexpression and structural analysis; no nutrient restriction. cross_nutrient: true evidence_location: Abstract; primary Results: Identification of the ACP–Lipid–ISD11 Motif [b5-met-cory2017] Structure of human Fe-S assembly subcomplex reveals unexpected cysteine desulfurase architecture and acyl-ACP-ISD11 interactions. (2017). https://pubmed.ncbi.nlm.nih.gov/28634302/ DOI: 10.1073/pnas.1702849114
Complete structured claim and evidence
Cardiac Ndufab1 deletion reduced assembled respiratory complexes I–III and supercomplexes in mouse heart mitochondria.
Mouse mitochondrial acyl carrier protein / Ndufab1 → Mitochondrial respiratory supercomplex assembly source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text lines 49–55; Fig. 3; Supplementary Figs. S6–S10
experimental_model
Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
exposure
Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays.
limitations
The FeS subunits of complexes II/III were preferentially affected, whereas broader complex-I subunit loss supports an additional assembly role. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Loss of the carrier impaired assembly of several respiratory complexes in mouse heart.
primary_references
[b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
tissue_or_cell_type
Heart mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 949–961
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft
### b5-met-heart-acp-complex-assembly Cardiac Ndufab1 deletion reduced assembled respiratory complexes I–III and supercomplexes in mouse heart mitochondria. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of the carrier impaired assembly of several respiratory complexes in mouse heart. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: The FeS subunits of complexes II/III were preferentially affected, whereas broader complex-I subunit loss supports an additional assembly role. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays. cross_nutrient: true evidence_location: Full text lines 49–55; Fig. 3; Supplementary Figs. S6–S10 [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
Complete structured claim and evidence
Cardiac Ndufab1 deletion lowered oxygen consumption supported by complex I-, II-, or III-linked substrates, while complex IV-linked respiration remained unchanged.
Mouse mitochondrial acyl carrier protein / Ndufab1 → ADP-stimulated mitochondrial oxygen consumption source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Full text lines 47–49; Fig. 3A
experimental_model
Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
exposure
Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays.
limitations
Isolated-mitochondria oxygen consumption does not measure nutrient absorption or human exercise capacity. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
The respiratory defect affected several upstream electron-transfer routes but spared the tested complex IV route.
primary_references
[b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
tissue_or_cell_type
Heart mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 963–975
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft
### b5-met-heart-acp-respiration Cardiac Ndufab1 deletion lowered oxygen consumption supported by complex I-, II-, or III-linked substrates, while complex IV-linked respiration remained unchanged. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The respiratory defect affected several upstream electron-transfer routes but spared the tested complex IV route. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: Isolated-mitochondria oxygen consumption does not measure nutrient absorption or human exercise capacity. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiac-specific genetic deletion; 6- and 16-week assembly assays, 6- and 10-week respiratory assays. cross_nutrient: false evidence_location: Full text lines 47–49; Fig. 3A [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
Complete structured claim and evidence
In the cardiac Ndufab1-knockout study, the measured mitochondrial protein lipoylation was not significantly changed despite respiratory defects.
Mouse mitochondrial acyl carrier protein / Ndufab1 → Mitochondrial protein lipoylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text line 47; Supplementary Fig. S4B
experimental_model
Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria
exposure
Cardiomyocyte-specific Ndufab1 deletion.
limitations
A null result for these measurements is not proof that all fatty-acid synthesis was intact. Different tissue, developmental timing and depletion conditions preclude a same-context contradiction with HEK293T cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Mouse heart respiratory failure occurred without the measured lipoylation defect seen in the cultured-cell study.
primary_references
[b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
tissue_or_cell_type
Heart mitochondria
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 977–989
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria · source_derived_draft · unverified_draft
### b5-met-heart-acp-lipoylation-spared In the cardiac Ndufab1-knockout study, the measured mitochondrial protein lipoylation was not significantly changed despite respiratory defects. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mouse heart respiratory failure occurred without the measured lipoylation defect seen in the cultured-cell study. organism: Mus musculus tissue_or_cell_type: Heart mitochondria experimental_model: Cardiomyocyte-specific Ndufab1 knockout mice and isolated heart mitochondria limitations: A null result for these measurements is not proof that all fatty-acid synthesis was intact. Different tissue, developmental timing and depletion conditions preclude a same-context contradiction with HEK293T cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiomyocyte-specific Ndufab1 deletion. cross_nutrient: true evidence_location: Full text line 47; Supplementary Fig. S4B [b5-met-ndufab2019] NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly. (2019). https://pubmed.ncbi.nlm.nih.gov/31366990/ DOI: 10.1038/s41422-019-0208-x
Complete structured claim and evidence
ACLY silencing reduced acetylation of the core histones assayed in HCT116 cells.
Human ATP-citrate lyase / ACLY → Core histone lysine acetylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
true
evidence_location
BioC text lines 11, 17, 51; Fig. 2A,E
experimental_model
ACLY siRNA versus control
exposure
72-hour siRNA treatment.
limitations
Tubulin acetylation was not comparably reduced. This is a source-specific cellular result, not a universal block of protein acetylation. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Histone acetylation depended partly on this source of acetyl-CoA in colon-cancer cells.
primary_references
[b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
tissue_or_cell_type
HCT116 cells and acid-extracted histones
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 991–1003
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ACLY siRNA versus control · source_derived_draft · unverified_draft
### b5-met-acly-hct-histones ACLY silencing reduced acetylation of the core histones assayed in HCT116 cells. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Histone acetylation depended partly on this source of acetyl-CoA in colon-cancer cells. organism: Homo sapiens tissue_or_cell_type: HCT116 cells and acid-extracted histones experimental_model: ACLY siRNA versus control limitations: Tubulin acetylation was not comparably reduced. This is a source-specific cellular result, not a universal block of protein acetylation. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 72-hour siRNA treatment. cross_nutrient: true evidence_location: BioC text lines 11, 17, 51; Fig. 2A,E [b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
Complete structured claim and evidence
Extracellular acetate restored histone acetylation in ACLY-silenced HCT116 cells in a dose-dependent manner that required AceCS1, now named ACSS2.
Acetate → Core histone lysine acetylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
evidence_location
BioC text lines 11, 51; Fig. 2A–B
experimental_model
ACLY and/or AceCS1 siRNA with acetate supplementation
exposure
0, 1 or 5 mM acetate for 24 hours before lysis after siRNA treatment.
limitations
The authors identify this acetate supply as supraphysiologic; it is not a dietary recommendation and does not show rescue of an absent CoA pool. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A second acetyl-CoA-producing route could compensate when enough acetate was supplied.
primary_references
[b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
tissue_or_cell_type
HCT116 cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1005–1017
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ACLY and/or AceCS1 siRNA with acetate supplementation · source_derived_draft · unverified_draft
### b5-met-acetate-acss2-histone-rescue Extracellular acetate restored histone acetylation in ACLY-silenced HCT116 cells in a dose-dependent manner that required AceCS1, now named ACSS2. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second acetyl-CoA-producing route could compensate when enough acetate was supplied. organism: Homo sapiens tissue_or_cell_type: HCT116 cells experimental_model: ACLY and/or AceCS1 siRNA with acetate supplementation limitations: The authors identify this acetate supply as supraphysiologic; it is not a dietary recommendation and does not show rescue of an absent CoA pool. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 0, 1 or 5 mM acetate for 24 hours before lysis after siRNA treatment. cross_nutrient: false evidence_location: BioC text lines 11, 51; Fig. 2A–B [b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
Complete structured claim and evidence
Serum-induced histone acetylation in immortalized mouse embryonic fibroblasts depended on glucose availability and was prevented by Acly silencing.
D-glucose → Core histone lysine acetylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
BioC text line 21; Fig. 3B–C
experimental_model
Serum stimulation with/without glucose and Acly siRNA
exposure
Experimental serum stimulation and glucose withdrawal; no selective pantothenate deprivation.
limitations
Glucose was the experimentally varied fuel. This is not evidence of B5 deficiency; cellular acetyl-CoA sources differ by context. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Mus musculus
plain_language
Glucose supply affected histone acetylation through an acetyl-CoA-producing enzyme in this cell model.
primary_references
[b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
tissue_or_cell_type
Immortalized mouse embryonic fibroblasts
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1019–1031
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Serum stimulation with/without glucose and Acly siRNA · source_derived_draft · unverified_draft
### b5-met-glucose-acly-histones Serum-induced histone acetylation in immortalized mouse embryonic fibroblasts depended on glucose availability and was prevented by Acly silencing. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glucose supply affected histone acetylation through an acetyl-CoA-producing enzyme in this cell model. organism: Mus musculus tissue_or_cell_type: Immortalized mouse embryonic fibroblasts experimental_model: Serum stimulation with/without glucose and Acly siRNA limitations: Glucose was the experimentally varied fuel. This is not evidence of B5 deficiency; cellular acetyl-CoA sources differ by context. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Experimental serum stimulation and glucose withdrawal; no selective pantothenate deprivation. cross_nutrient: true evidence_location: BioC text line 21; Fig. 3B–C [b5-met-chromatin2009] ATP-citrate lyase links cellular metabolism to histone acetylation. (2009). https://pubmed.ncbi.nlm.nih.gov/19461003/ DOI: 10.1126/science.1164097
Complete structured claim and evidence
The inactive human ACC1 filament structure resolved acetyl-CoA in a pocket at the carboxyltransferase dimer interface.
Acetyl-CoA → Human acetyl-CoA carboxylase 1 / ACACA source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Full text lines 101, 131; Fig. 4B
experimental_model
Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM
exposure
Substrate preparation contained 10 mM acetyl-CoA, 25 mM bicarbonate, 10 mM MgCl2 and 10 mM ATP; cryo-EM preparation conditions.
limitations
Ligand occupancy in an inactive structure is not an activity or dietary-repletion assay. Biotin density was not resolved in this map. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Acetyl-CoA binds the biotin-dependent carboxylase even in a structurally inactive state.
primary_references
[b5-met-acc2024] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
tissue_or_cell_type
Purified endogenous Expi293F ACC1
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1033–1045
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM · source_derived_draft · unverified_draft
### b5-met-acc-acetylcoa-binding The inactive human ACC1 filament structure resolved acetyl-CoA in a pocket at the carboxyltransferase dimer interface. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acetyl-CoA binds the biotin-dependent carboxylase even in a structurally inactive state. organism: Homo sapiens tissue_or_cell_type: Purified endogenous Expi293F ACC1 experimental_model: Endogenous human ACC1 purified from Expi293F cells and analyzed by cryo-EM limitations: Ligand occupancy in an inactive structure is not an activity or dietary-repletion assay. Biotin density was not resolved in this map. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Substrate preparation contained 10 mM acetyl-CoA, 25 mM bicarbonate, 10 mM MgCl2 and 10 mM ATP; cryo-EM preparation conditions. cross_nutrient: true evidence_location: Full text lines 101, 131; Fig. 4B [b5-met-acc2024] Filament structures unveil the dynamic organization of human acetyl-CoA carboxylase. (2024). https://pubmed.ncbi.nlm.nih.gov/39383219/ DOI: 10.1126/sciadv.ado4880
Complete structured claim and evidence
Hydrogen peroxide exposure induced DTT-sensitive protein CoAlation in isolated rat cardiomyocytes and perfused rat hearts.
Hydrogen peroxide → Protein cysteine CoAlation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text lines 105–107; Fig. 1B–D
experimental_model
Primary cardiomyocyte exposure and Langendorff-perfused rat hearts
exposure
Cardiomyocytes: 1–100 micromolar H2O2, 30 minutes; perfused hearts: 100 micromolar H2O2, 20 minutes.
limitations
DTT sensitivity supports mixed disulfides. Antioxidant protection or improved organ function was not established by this endpoint. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Rattus norvegicus
plain_language
Oxidative stress caused CoA to form reversible bonds with protein cysteines.
primary_references
[b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
tissue_or_cell_type
Adult cardiomyocytes and isolated heart
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1047–1059
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary cardiomyocyte exposure and Langendorff-perfused rat hearts · source_derived_draft · unverified_draft
### b5-met-oxidant-coalation Hydrogen peroxide exposure induced DTT-sensitive protein CoAlation in isolated rat cardiomyocytes and perfused rat hearts. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidative stress caused CoA to form reversible bonds with protein cysteines. organism: Rattus norvegicus tissue_or_cell_type: Adult cardiomyocytes and isolated heart experimental_model: Primary cardiomyocyte exposure and Langendorff-perfused rat hearts limitations: DTT sensitivity supports mixed disulfides. Antioxidant protection or improved organ function was not established by this endpoint. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Cardiomyocytes: 1–100 micromolar H2O2, 30 minutes; perfused hearts: 100 micromolar H2O2, 20 minutes. cross_nutrient: false evidence_location: Full text lines 105–107; Fig. 1B–D [b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
Complete structured claim and evidence
After removal of hydrogen peroxide from HEK293/Pank1beta cultures, induced protein CoAlation declined within 5 minutes and returned to baseline within 90 minutes.
Protein cysteine–CoA mixed disulfides → Protein cysteine CoAlation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text line 115; Fig. 2C
experimental_model
Oxidant washout in HEK293 cells stably overexpressing Pank1beta
exposure
500 micromolar H2O2 for 60 minutes, then recovery in complete growth medium.
limitations
The removal mechanism was not identified; engineered high-CoA cells are not ordinary circulating blood cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The CoA modification receded when the oxidative exposure ended.
primary_references
[b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
tissue_or_cell_type
Engineered HEK293 cultures
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1061–1073
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oxidant washout in HEK293 cells stably overexpressing Pank1beta · source_derived_draft · unverified_draft
### b5-met-coalation-reversal After removal of hydrogen peroxide from HEK293/Pank1beta cultures, induced protein CoAlation declined within 5 minutes and returned to baseline within 90 minutes. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The CoA modification receded when the oxidative exposure ended. organism: Homo sapiens tissue_or_cell_type: Engineered HEK293 cultures experimental_model: Oxidant washout in HEK293 cells stably overexpressing Pank1beta limitations: The removal mechanism was not identified; engineered high-CoA cells are not ordinary circulating blood cells. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 500 micromolar H2O2 for 60 minutes, then recovery in complete growth medium. cross_nutrient: false evidence_location: Full text line 115; Fig. 2C [b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
Complete structured claim and evidence
Vitamin C pretreatment reduced diamide-induced anti-CoA protein immunoreactivity by approximately 50% in HEK293/Pank1beta cells.
L-Ascorbic acid → Protein cysteine CoAlation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Full text lines 29 and 117; Fig. 2E
experimental_model
Antioxidant pretreatment of engineered HEK293/Pank1beta cells
exposure
1 mM vitamin C for 2 hours before 0.5 mM diamide for 30 minutes.
limitations
The endpoint is protein anti-CoA immunoreactivity, not clinical benefit; lower CoAlation is not assumed universally beneficial. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Vitamin C exposure blunted the measured CoA protein modification during this experimental oxidative challenge.
primary_references
[b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
tissue_or_cell_type
Engineered HEK293 cultures
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1075–1087
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Antioxidant pretreatment of engineered HEK293/Pank1beta cells · source_derived_draft · unverified_draft
### b5-met-vitc-coalation Vitamin C pretreatment reduced diamide-induced anti-CoA protein immunoreactivity by approximately 50% in HEK293/Pank1beta cells. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C exposure blunted the measured CoA protein modification during this experimental oxidative challenge. organism: Homo sapiens tissue_or_cell_type: Engineered HEK293 cultures experimental_model: Antioxidant pretreatment of engineered HEK293/Pank1beta cells limitations: The endpoint is protein anti-CoA immunoreactivity, not clinical benefit; lower CoAlation is not assumed universally beneficial. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 1 mM vitamin C for 2 hours before 0.5 mM diamide for 30 minutes. cross_nutrient: true evidence_location: Full text lines 29 and 117; Fig. 2E [b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
Complete structured claim and evidence
In-vitro CoAlation of immunoprecipitated recombinant PDK2 reduced its phosphorylation of PDH E1, and DTT restored kinase activity.
Coenzyme A disulfide → Human pyruvate dehydrogenase kinase 2 / PDK2 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Full text lines 33, 61 and 141; Fig. 6D
experimental_model
FLAG-PDK2 expressed in HEK293 cells, immunoprecipitated and assayed with porcine-heart PDH
exposure
1 mM CoA disulfide preincubation for 20 minutes; PDH phosphorylation assay with/without 2 mM DTT.
limitations
CoA disulfide is distinct from reduced CoA. The assay does not establish net mitochondrial PDH flux or a supplementation effect in vivo. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Human PDK2; Sus scrofa PDH assay substrate
plain_language
Adding CoA through a disulfide bond reversibly inhibited the kinase that regulates pyruvate dehydrogenase.
primary_references
[b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
tissue_or_cell_type
Cell-free kinase assay
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1089–1101
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FLAG-PDK2 expressed in HEK293 cells, immunoprecipitated and assayed with porcine-heart PDH · source_derived_draft · unverified_draft
### b5-met-pdk2-coalation-inhibition In-vitro CoAlation of immunoprecipitated recombinant PDK2 reduced its phosphorylation of PDH E1, and DTT restored kinase activity. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding CoA through a disulfide bond reversibly inhibited the kinase that regulates pyruvate dehydrogenase. organism: Human PDK2; Sus scrofa PDH assay substrate tissue_or_cell_type: Cell-free kinase assay experimental_model: FLAG-PDK2 expressed in HEK293 cells, immunoprecipitated and assayed with porcine-heart PDH limitations: CoA disulfide is distinct from reduced CoA. The assay does not establish net mitochondrial PDH flux or a supplementation effect in vivo. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: 1 mM CoA disulfide preincubation for 20 minutes; PDH phosphorylation assay with/without 2 mM DTT. cross_nutrient: false evidence_location: Full text lines 33, 61 and 141; Fig. 6D [b5-met-coalation2017] Protein CoAlation: a redox-regulated protein modification by coenzyme A in mammalian cells. (2017). https://pubmed.ncbi.nlm.nih.gov/28341808/ DOI: 10.1042/bcj20170129
Complete structured claim and evidence
A pantothenate-free diet reduced free CoA measured in human HCI002 breast-cancer xenografts grown in mice.
Pantothenate (vitamin B5) → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Full text lines 123–125, 173, 229; Fig. 4F; Extended Data Fig. 5G–H
experimental_model
Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts
exposure
Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice.
limitations
The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Human HCI002 grafts in Mus musculus hosts
plain_language
Direct B5 restriction lowered the tumor CoA pool in this particular graft model.
primary_references
[b5-met-myc2024] Vitamin B5 supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7
tissue_or_cell_type
Orthotopic HCI002 tumor tissue
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1103–1115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts · source_derived_draft · unverified_draft
### b5-met-diet-hci002-coa A pantothenate-free diet reduced free CoA measured in human HCI002 breast-cancer xenografts grown in mice. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Direct B5 restriction lowered the tumor CoA pool in this particular graft model. organism: Human HCI002 grafts in Mus musculus hosts tissue_or_cell_type: Orthotopic HCI002 tumor tissue experimental_model: Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts limitations: The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. cross_nutrient: false evidence_location: Full text lines 123–125, 173, 229; Fig. 4F; Extended Data Fig. 5G–H [b5-met-myc2024] Vitamin B5 supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7
Complete structured claim and evidence
Pantothenate deprivation reduced the amount of glucose-derived carbon-13-labeled acetyl-CoA in HCI002 xenografts.
Pantothenate (vitamin B5) → Acetyl-CoA source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Full text lines 107, 123–125; Fig. 4F–G; Extended Data Fig. 5G–H
experimental_model
Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing
exposure
Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. Carbon-13 glucose tracing followed by LC-MS.
limitations
The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Human HCI002 grafts in Mus musculus hosts
plain_language
B5 restriction also reduced the measured labeled acetyl-CoA formed from glucose in these tumors.
primary_references
[b5-met-myc2024] Vitamin B5 supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7
tissue_or_cell_type
Orthotopic HCI002 tumor tissue
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1117–1129
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing · source_derived_draft · unverified_draft
### b5-met-diet-hci002-acetylcoa Pantothenate deprivation reduced the amount of glucose-derived carbon-13-labeled acetyl-CoA in HCI002 xenografts. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5 restriction also reduced the measured labeled acetyl-CoA formed from glucose in these tumors. organism: Human HCI002 grafts in Mus musculus hosts tissue_or_cell_type: Orthotopic HCI002 tumor tissue experimental_model: Matched PA-free/control diets in NOD/Scid mice bearing orthotopic human HCI002 breast-cancer xenografts with carbon-13 glucose tracing limitations: The same paper found no significant fall in the corresponding CoA/acetyl-CoA pools in WMmix tumors. Tumor concentration and tracer labeling do not establish universal CoA depletion or a human anticancer diet; cellular composition and pool size can affect the measured label. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Diets introduced at 6 weeks of age, progressively over 4 days; typically 5 weeks on the assigned diet before implantation and continued until collection. PA absence verified by LC-MS; control was composition-matched with PA added. Control n=7, PA-free n=8 tumors from independent mice. Carbon-13 glucose tracing followed by LC-MS. cross_nutrient: true evidence_location: Full text lines 107, 123–125; Fig. 4F–G; Extended Data Fig. 5G–H [b5-met-myc2024] Vitamin B5 supports MYC oncogenic metabolism and tumor progression in breast cancer. (2023). https://pubmed.ncbi.nlm.nih.gov/37946084/ DOI: 10.1038/s42255-023-00915-7
Complete structured claim and evidence
Rats fed the pantothenate-deficient diet retained control-level tissue CoA despite more than 90% lower pantothenate in heart, kidney, gastrocnemius and testes and about 70% lower liver pantothenate.
Pantothenate (vitamin B5) → Coenzyme A source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary abstract, first four sentences
experimental_model
Rat pantothenate-deficient versus regular-diet feeding experiment
exposure
Pantothenic-acid-deficient diet; concentration and feeding duration unavailable in the abstract.
limitations
Whole-tissue CoA measurement does not establish unchanged subcellular pools or flux. Growth was impaired, so maintained CoA did not show nutritional adequacy. Different tissues/models from the tumor study do not constitute a same-context contradiction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Rattus norvegicus
plain_language
Large drops in tissue B5 did not necessarily deplete the measured CoA pool in this rat experiment.
primary_references
[b5-met-rat1982] Coenzyme A metabolism in pantothenic acid-deficient rats. (1982). https://pubmed.ncbi.nlm.nih.gov/7086543/ DOI: 10.1093/jn/112.6.1144
tissue_or_cell_type
Heart, kidney, gastrocnemius, testes and liver
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1131–1143
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat pantothenate-deficient versus regular-diet feeding experiment · source_derived_draft · unverified_draft
### b5-met-rat-diet-coa-preserved Rats fed the pantothenate-deficient diet retained control-level tissue CoA despite more than 90% lower pantothenate in heart, kidney, gastrocnemius and testes and about 70% lower liver pantothenate. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Large drops in tissue B5 did not necessarily deplete the measured CoA pool in this rat experiment. organism: Rattus norvegicus tissue_or_cell_type: Heart, kidney, gastrocnemius, testes and liver experimental_model: Rat pantothenate-deficient versus regular-diet feeding experiment limitations: Whole-tissue CoA measurement does not establish unchanged subcellular pools or flux. Growth was impaired, so maintained CoA did not show nutritional adequacy. Different tissues/models from the tumor study do not constitute a same-context contradiction. This experiment does not establish a dietary pantothenate threshold or benefit from B5 supplementation. exposure: Pantothenic-acid-deficient diet; concentration and feeding duration unavailable in the abstract. cross_nutrient: false evidence_location: Primary abstract, first four sentences [b5-met-rat1982] Coenzyme A metabolism in pantothenic acid-deficient rats. (1982). https://pubmed.ncbi.nlm.nih.gov/7086543/ DOI: 10.1093/jn/112.6.1144
Complete structured claim and evidence
In the 1958 six-man study, the two men on the B5-devoid diet developed fatigue, behavioral and gastrointestinal complaints and impaired coordination after the antagonist-treated pair; the supplemented controls remained well.
Pantothenate (vitamin B5) → Clinical symptoms during pantothenate depletion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary PDF pp.1643–1654; design, results and discussion.
experimental_model
Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
exposure
Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
limitations
Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Prolonged dietary depletion produced symptoms in this small controlled study, with earlier changes when an antagonist was also given.
primary_references
[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
tissue_or_cell_type
Whole-person symptoms, serum and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1145–1157
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft
### b5-clin-diet-symptoms In the 1958 six-man study, the two men on the B5-devoid diet developed fatigue, behavioral and gastrointestinal complaints and impaired coordination after the antagonist-treated pair; the supplemented controls remained well. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prolonged dietary depletion produced symptoms in this small controlled study, with earlier changes when an antagonist was also given. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
Complete structured claim and evidence
Urinary pantothenic acid approached zero after the eleventh week of the deficient diet in the 1958 experiment.
Pantothenate (vitamin B5) → Urinary pantothenate excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary PDF pp.1643–1654; design, results and discussion.
experimental_model
Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
exposure
Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
limitations
Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Urinary B5 fell substantially during sustained dietary depletion.
primary_references
[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
tissue_or_cell_type
Whole-person symptoms, serum and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1159–1171
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft
### b5-clin-diet-urine Urinary pantothenic acid approached zero after the eleventh week of the deficient diet in the 1958 experiment. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urinary B5 fell substantially during sustained dietary depletion. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
Complete structured claim and evidence
The 1958 depletion study found an impaired eosinopenic response to ACTH, while urinary 17-ketosteroid excretion remained normal; the authors did not interpret this pattern as sufficient evidence of adrenal cortical hypofunction.
Pantothenate (vitamin B5) → Eosinopenic response to ACTH source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary PDF pp.1643–1654; design, results and discussion.
experimental_model
Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
exposure
Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
limitations
Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The altered hormone-response test did not establish adrenal failure.
primary_references
[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
tissue_or_cell_type
Whole-person symptoms, serum and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1173–1185
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft
### b5-clin-acth-not-adrenal-diagnosis The 1958 depletion study found an impaired eosinopenic response to ACTH, while urinary 17-ketosteroid excretion remained normal; the authors did not interpret this pattern as sufficient evidence of adrenal cortical hypofunction. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The altered hormone-response test did not establish adrenal failure. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
Complete structured claim and evidence
On the experimental formula, men receiving 20.5 mEq/day potassium had serum potassium near the lower normal limit, while an extra 10.8 mEq/day maintained somewhat higher values across the paired B5 regimens.
Potassium ion → Serum or plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
evidence_location
Primary PDF pp.1643–1654; design, results and discussion.
experimental_model
Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
exposure
Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
limitations
Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Potassium supply affected the blood result independently of how the B5 groups were assigned.
primary_references
[b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
tissue_or_cell_type
Whole-person symptoms, serum and urine
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1187–1199
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft
### b5-clin-potassium-context On the experimental formula, men receiving 20.5 mEq/day potassium had serum potassium near the lower normal limit, while an extra 10.8 mEq/day maintained somewhat higher values across the paired B5 regimens. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium supply affected the blood result independently of how the B5 groups were assigned. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: true evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
Complete structured claim and evidence
In the four-man normal-diet experiment, the intermediate-antagonist subject developed gastrointestinal and neurological symptoms, while the highest-exposure subject had mainly a transient tremor; the control and lowest-exposure subject remained relatively well.
Omega-methyl pantothenic acid → Clinical symptoms during pantothenate depletion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary PDF pp.1421–1425, especially Results and Summary.
experimental_model
Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet
exposure
One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal.
limitations
Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. The interindividual pattern is not a monotonic dose-response or a direct assay of a specific PANK isoform.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Blocking vitamin use experimentally produced variable illness despite a normal diet.
primary_references
[b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
tissue_or_cell_type
Whole-person clinical symptoms and functional tests
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1201–1213
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet · source_derived_draft · unverified_draft
### b5-clin-antagonist-variable-symptoms In the four-man normal-diet experiment, the intermediate-antagonist subject developed gastrointestinal and neurological symptoms, while the highest-exposure subject had mainly a transient tremor; the control and lowest-exposure subject remained relatively well. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking vitamin use experimentally produced variable illness despite a normal diet. organism: Homo sapiens tissue_or_cell_type: Whole-person clinical symptoms and functional tests experimental_model: Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet limitations: Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. The interindividual pattern is not a monotonic dose-response or a direct assay of a specific PANK isoform. exposure: One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal. cross_nutrient: false evidence_location: Primary PDF pp.1421–1425, especially Results and Summary. [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
Complete structured claim and evidence
Abnormal ACTH-associated eosinopenic responses in the two more heavily exposed men recovered after the antagonist was stopped and pantothenic acid was administered.
Pantothenate (vitamin B5) → Eosinopenic response to ACTH source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary PDF pp.1421–1425, especially Results and Summary.
experimental_model
Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet
exposure
One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal.
limitations
Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Recovery followed both removal of the antagonist and vitamin treatment.
primary_references
[b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
tissue_or_cell_type
Whole-person clinical symptoms and functional tests
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1215–1227
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet · source_derived_draft · unverified_draft
### b5-clin-antagonist-recovery Abnormal ACTH-associated eosinopenic responses in the two more heavily exposed men recovered after the antagonist was stopped and pantothenic acid was administered. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recovery followed both removal of the antagonist and vitamin treatment. organism: Homo sapiens tissue_or_cell_type: Whole-person clinical symptoms and functional tests experimental_model: Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet limitations: Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration. exposure: One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal. cross_nutrient: false evidence_location: Primary PDF pp.1421–1425, especially Results and Summary. [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
Complete structured claim and evidence
After 63 days, mean urinary pantothenate fell from 3.05 to 0.79 mg/day in the unsupplemented men; it rose from 3.95 to 5.84 mg/day with 10 mg/day supplementation.
Pantothenate (vitamin B5) → Urinary pantothenate excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.
experimental_model
Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented
exposure
Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.
limitations
Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The authors reported no defined clinical deficiency syndrome over nine weeks, although listlessness and fatigue were noted near the end.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Urinary excretion responded strongly to whether B5 was supplied.
primary_references
[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
tissue_or_cell_type
Urine and whole blood; nitrogen balance
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1229–1241
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft
### b5-clin-urine-intake-response After 63 days, mean urinary pantothenate fell from 3.05 to 0.79 mg/day in the unsupplemented men; it rose from 3.95 to 5.84 mg/day with 10 mg/day supplementation. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urinary excretion responded strongly to whether B5 was supplied. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The authors reported no defined clinical deficiency syndrome over nine weeks, although listlessness and fatigue were noted near the end. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
Complete structured claim and evidence
Whole-blood pantothenate decreased in the unsupplemented group and remained broadly stable in the supplemented group, but separated intake groups less readily than urinary excretion.
Pantothenate (vitamin B5) → Blood pantothenate concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.
experimental_model
Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented
exposure
Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.
limitations
Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Blood and urine measurements did not respond identically to dietary depletion.
primary_references
[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
tissue_or_cell_type
Urine and whole blood; nitrogen balance
trigger_kind
biomarker_context Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1243–1255
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### b5-clin-blood-intake-response Whole-blood pantothenate decreased in the unsupplemented group and remained broadly stable in the supplemented group, but separated intake groups less readily than urinary excretion. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood and urine measurements did not respond identically to dietary depletion. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
Complete structured claim and evidence
On the first 100 mg B5 loading day, prior unsupplemented subjects excreted about 37 mg and supplemented subjects about 52 mg in urine; by day seven the means were about 59 and 62 mg.
Calcium pantothenate → Urinary pantothenate excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.
experimental_model
Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented
exposure
Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.
limitations
Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The paper called the unexcreted fractions 63% and 48% retained on day one. These calculations do not directly measure absorption, tissue storage or CoA synthesis.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Prior intake changed urinary recovery of a loading dose, and the groups became more similar over a week.
primary_references
[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
tissue_or_cell_type
Urine and whole blood; nitrogen balance
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1257–1269
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft
### b5-clin-loading-urinary-recovery On the first 100 mg B5 loading day, prior unsupplemented subjects excreted about 37 mg and supplemented subjects about 52 mg in urine; by day seven the means were about 59 and 62 mg. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prior intake changed urinary recovery of a loading dose, and the groups became more similar over a week. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. The paper called the unexcreted fractions 63% and 48% retained on day one. These calculations do not directly measure absorption, tissue storage or CoA synthesis. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
Complete structured claim and evidence
Mean nitrogen balance was numerically higher with 10 mg/day B5 than without supplementation, but the between-group difference was not statistically significant.
Calcium pantothenate → Whole-body nitrogen balance source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345.
experimental_model
Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented
exposure
Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days.
limitations
Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. A numerical trend does not establish enhanced protein synthesis or an amino-acid repletion gate.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
This study did not demonstrate a significant improvement in nitrogen balance.
primary_references
[b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
tissue_or_cell_type
Urine and whole blood; nitrogen balance
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1271–1283
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented · source_derived_draft · unverified_draft
### b5-clin-nitrogen-not-significant Mean nitrogen balance was numerically higher with 10 mg/day B5 than without supplementation, but the between-group difference was not statistically significant. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: This study did not demonstrate a significant improvement in nitrogen balance. organism: Homo sapiens tissue_or_cell_type: Urine and whole blood; nitrogen balance experimental_model: Controlled 84-day feeding experiment in ten adult male inmates aged 27–33; six unsupplemented and four supplemented limitations: Table 1 and the abstract distinguish unsupplemented and supplemented groups; one Methods sentence incorrectly says all received 10 mg. The table was visually checked. Historical assay and small cohort; the reported retention calculation is not direct measurement of intestinal absorption or tissue CoA. A numerical trend does not establish enhanced protein synthesis or an amino-acid repletion gate. exposure: Nine-week/63-day experimental diet essentially free of B5 versus 10 mg/day B5 as calcium pantothenate; both groups then received 100 mg/day for seven days. cross_nutrient: false evidence_location: Primary PDF Table 1 visually checked; Tables 3–4 and Results pp.341–345. [b5-clin-fry1976] Metabolic response to a pantothenic acid deficient diet in humans. (1976). https://pubmed.ncbi.nlm.nih.gov/1011047/ DOI: 10.3177/jnsv.22.339
Complete structured claim and evidence
In 63 adolescents, recorded pantothenate intake correlated with urinary excretion (P<0.001); erythrocyte pantothenate also correlated with intake and urinary excretion.
Pantothenate (vitamin B5) → Urinary pantothenate excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Observational study of 63 healthy adolescents
exposure
Four-day diet records; pantothenate measured by radioimmunoassay.
limitations
Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Urine and red-cell measurements tracked intake in this group.
primary_references
[b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931
tissue_or_cell_type
Diet records, urine, whole blood and erythrocytes
trigger_kind
biomarker_context Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1285–1297
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 63 healthy adolescents · source_derived_draft · unverified_draft
### b5-clin-adolescent-urine-correlation In 63 adolescents, recorded pantothenate intake correlated with urinary excretion (P<0.001); erythrocyte pantothenate also correlated with intake and urinary excretion. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urine and red-cell measurements tracked intake in this group. organism: Homo sapiens tissue_or_cell_type: Diet records, urine, whole blood and erythrocytes experimental_model: Observational study of 63 healthy adolescents limitations: Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. exposure: Four-day diet records; pantothenate measured by radioimmunoassay. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931
Complete structured claim and evidence
Although 49% of female and 15% of male adolescents recorded intakes below 4 mg/day, group-average blood concentrations were within the ranges reported for comparison populations.
Pantothenate (vitamin B5) → Blood pantothenate concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Observational study of 63 healthy adolescents
exposure
Four-day diet records; pantothenate measured by radioimmunoassay.
limitations
Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. Below 4 mg/day was a historical descriptive cutoff, not a validated individual deficiency threshold.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A low short diet record did not reliably identify a low group-average blood value.
primary_references
[b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931
tissue_or_cell_type
Diet records, urine, whole blood and erythrocytes
trigger_kind
biomarker_context Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1299–1311
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 63 healthy adolescents · source_derived_draft · unverified_draft
### b5-clin-adolescent-intake-blood-discordance Although 49% of female and 15% of male adolescents recorded intakes below 4 mg/day, group-average blood concentrations were within the ranges reported for comparison populations. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low short diet record did not reliably identify a low group-average blood value. organism: Homo sapiens tissue_or_cell_type: Diet records, urine, whole blood and erythrocytes experimental_model: Observational study of 63 healthy adolescents limitations: Correlations and comparisons with other populations do not establish cellular adequacy, an individual requirement or a diagnostic threshold. Historical recommended-intake discussion is not used as current guidance. Below 4 mg/day was a historical descriptive cutoff, not a validated individual deficiency threshold. exposure: Four-day diet records; pantothenate measured by radioimmunoassay. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-eissenstat1986] Pantothenic acid status of adolescents. (1986). https://pubmed.ncbi.nlm.nih.gov/3788840/ DOI: 10.1093/ajcn/44.6.931
Complete structured claim and evidence
In the elderly cohort, free pantothenic acid was detected in urine, whereas the measured phosphoderivative fraction was not; microbiological and radioimmunoassay estimates correlated at r=0.91.
Urinary pantothenate excretion → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Observational study of 91 adults aged at least 65, including institutionalized and community participants
exposure
Microbiological and radioimmunoassay analyses of free and derivative pantothenate fractions.
limitations
Assay-specific findings; urinary free pantothenate is distinct from intracellular CoA and its acyl derivatives.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The urinary assay mostly described free vitamin, not the cell’s activated CoA pool.
primary_references
[b5-clin-tarr1981] Pantothenic acid nutritional status in the elderly--institutionalized and noninstitutionalized. (1981). https://pubmed.ncbi.nlm.nih.gov/7025609/ DOI: 10.1093/ajcn/34.9.1736
tissue_or_cell_type
Fasting blood, 24-hour urine and seven-day diet records
trigger_kind
biomarker_context Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1313–1325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational study of 91 adults aged at least 65, including institutionalized and community participants · source_derived_draft · unverified_draft
### b5-clin-urinary-species In the elderly cohort, free pantothenic acid was detected in urine, whereas the measured phosphoderivative fraction was not; microbiological and radioimmunoassay estimates correlated at r=0.91. Condition category: biomarker_context nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The urinary assay mostly described free vitamin, not the cell’s activated CoA pool. organism: Homo sapiens tissue_or_cell_type: Fasting blood, 24-hour urine and seven-day diet records experimental_model: Observational study of 91 adults aged at least 65, including institutionalized and community participants limitations: Assay-specific findings; urinary free pantothenate is distinct from intracellular CoA and its acyl derivatives. exposure: Microbiological and radioimmunoassay analyses of free and derivative pantothenate fractions. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-tarr1981] Pantothenic acid nutritional status in the elderly--institutionalized and noninstitutionalized. (1981). https://pubmed.ncbi.nlm.nih.gov/7025609/ DOI: 10.1093/ajcn/34.9.1736
Complete structured claim and evidence
The five men receiving B5/B6-deficient diet plus both antagonists failed to respond to tetanus and typhoid O immunization and had little typhoid H response.
Pantothenate (vitamin B5) → Antibody response to tetanus and typhoid immunization source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
experimental_model
Historical two-stage combined B5/B6 depletion experiment in male volunteers
exposure
First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
limitations
Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Combined depletion and antivitamins impaired some antibody responses.
primary_references
[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
tissue_or_cell_type
Immunization responses and serum proteins
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1327–1339
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft
### b5-clin-combined-antibody-loss The five men receiving B5/B6-deficient diet plus both antagonists failed to respond to tetanus and typhoid O immunization and had little typhoid H response. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Combined depletion and antivitamins impaired some antibody responses. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
Complete structured claim and evidence
The same five men retained strong antibody responses to polio immunization despite their impaired tetanus and typhoid responses.
Pantothenate (vitamin B5) → Antibody response to polio immunization source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
experimental_model
Historical two-stage combined B5/B6 depletion experiment in male volunteers
exposure
First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
limitations
Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The immune impairment did not affect every tested antigen equally.
primary_references
[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
tissue_or_cell_type
Immunization responses and serum proteins
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1341–1353
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft
### b5-clin-combined-polio-preserved The same five men retained strong antibody responses to polio immunization despite their impaired tetanus and typhoid responses. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The immune impairment did not affect every tested antigen equally. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
Complete structured claim and evidence
After vitamins were restored and the five subjects were reimmunized, tetanus and typhoid antibody responses were reported as normal.
Pantothenate (vitamin B5) → Antibody response to tetanus and typhoid immunization source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
experimental_model
Historical two-stage combined B5/B6 depletion experiment in male volunteers
exposure
First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
limitations
Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Responses recovered after combined vitamin restoration and another immunization.
primary_references
[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
tissue_or_cell_type
Immunization responses and serum proteins
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1355–1367
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft
### b5-clin-combined-immune-recovery After vitamins were restored and the five subjects were reimmunized, tetanus and typhoid antibody responses were reported as normal. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Responses recovered after combined vitamin restoration and another immunization. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. This is not a blinded comparison of B5 alone, B6 alone or their interaction. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
Complete structured claim and evidence
The two men receiving the B5/B6-deficient diet without antagonists in the first stage showed minor abnormalities but no impairment of antibody production in that stage.
Pantothenate (vitamin B5) → Antibody response to tetanus and typhoid immunization source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
true
evidence_location
Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved.
experimental_model
Historical two-stage combined B5/B6 depletion experiment in male volunteers
exposure
First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary.
limitations
Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Diet-only restriction gave a different result from the later antivitamin regimen.
primary_references
[b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
tissue_or_cell_type
Immunization responses and serum proteins
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1369–1381
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical two-stage combined B5/B6 depletion experiment in male volunteers · source_derived_draft · unverified_draft
### b5-clin-diet-only-immune-result The two men receiving the B5/B6-deficient diet without antagonists in the first stage showed minor abnormalities but no impairment of antibody production in that stage. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Diet-only restriction gave a different result from the later antivitamin regimen. organism: Homo sapiens tissue_or_cell_type: Immunization responses and serum proteins experimental_model: Historical two-stage combined B5/B6 depletion experiment in male volunteers limitations: Combined nutrient restriction plus antivitamins cannot identify the separate contribution of B5 or B6, a synergistic effect, or a universal immune defect. Reimmunization also changes prior antigen exposure. Only two subjects; not proof that prolonged isolated dietary deficiency cannot impair immunity. exposure: First stage: two controls, two diet-only deficient men and one receiving diet plus both antagonists. Second stage: five men received B5/B6-deficient diet plus omega-methyl pantothenic acid and desoxypyridoxine; exact doses not available in the publisher summary. cross_nutrient: true evidence_location: Publisher primary Summary at https://www.sciencedirect.com/science/article/abs/pii/S0002916523345945 ; full article not retrieved. [b5-clin-hodges1962] Factors affecting human antibody response. V. Combined deficiencies of pantothenic acid and pyridoxine. (1962). https://pubmed.ncbi.nlm.nih.gov/13907960/ DOI: 10.1093/ajcn/11.3.187
Complete structured claim and evidence
At 16 weeks, the pantethine trial reported a 4 mg/dL (4%) LDL-C reduction from baseline, with a significant comparison against placebo while both groups followed the TLC diet.
Pantethine → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk
exposure
TLC diet begun four weeks before randomization and continued; 60 per group; pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16.
limitations
Lipid markers rather than cardiovascular events; pantethine is a derivative, not dietary B5 repletion. Absolute changes were small. Industry-associated authors; full methods were not retrieved. The 4 mg/dL figure is the reported change from baseline, not a separately verified adjusted between-group estimate.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Pantethine produced a modest LDL reduction in this trial.
primary_references
[b5-clin-rumberger2011] Pantethine, a derivative of vitamin B(5) used as a nutritional supplement, favorably alters low-density lipoprotein cholesterol metabolism in low- to moderate-cardiovascular risk North American subjects: a triple-blinded placebo and diet-controlled investigation. (2011). https://pubmed.ncbi.nlm.nih.gov/21925346/ DOI: 10.1016/j.nutres.2011.08.001
tissue_or_cell_type
Circulating lipids and lipoproteins
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1383–1395
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk · source_derived_draft · unverified_draft
### b5-clin-pantethine-ldl-2011 At 16 weeks, the pantethine trial reported a 4 mg/dL (4%) LDL-C reduction from baseline, with a significant comparison against placebo while both groups followed the TLC diet. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pantethine produced a modest LDL reduction in this trial. organism: Homo sapiens tissue_or_cell_type: Circulating lipids and lipoproteins experimental_model: Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk limitations: Lipid markers rather than cardiovascular events; pantethine is a derivative, not dietary B5 repletion. Absolute changes were small. Industry-associated authors; full methods were not retrieved. The 4 mg/dL figure is the reported change from baseline, not a separately verified adjusted between-group estimate. exposure: TLC diet begun four weeks before randomization and continued; 60 per group; pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-rumberger2011] Pantethine, a derivative of vitamin B(5) used as a nutritional supplement, favorably alters low-density lipoprotein cholesterol metabolism in low- to moderate-cardiovascular risk North American subjects: a triple-blinded placebo and diet-controlled investigation. (2011). https://pubmed.ncbi.nlm.nih.gov/21925346/ DOI: 10.1016/j.nutres.2011.08.001
Complete structured claim and evidence
The same trial reported a 4 mg/dL (5%) apolipoprotein B reduction from baseline at week 16 and a significant comparison with placebo.
Pantethine → Circulating apolipoprotein B concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk
exposure
TLC diet begun four weeks before randomization and continued; 60 per group; pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16.
limitations
Lipid markers rather than cardiovascular events; pantethine is a derivative, not dietary B5 repletion. Absolute changes were small. Industry-associated authors; full methods were not retrieved.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
A related lipoprotein marker also decreased modestly.
primary_references
[b5-clin-rumberger2011] Pantethine, a derivative of vitamin B(5) used as a nutritional supplement, favorably alters low-density lipoprotein cholesterol metabolism in low- to moderate-cardiovascular risk North American subjects: a triple-blinded placebo and diet-controlled investigation. (2011). https://pubmed.ncbi.nlm.nih.gov/21925346/ DOI: 10.1016/j.nutres.2011.08.001
tissue_or_cell_type
Circulating lipids and lipoproteins
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1397–1409
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk · source_derived_draft · unverified_draft
### b5-clin-pantethine-apob-2011 The same trial reported a 4 mg/dL (5%) apolipoprotein B reduction from baseline at week 16 and a significant comparison with placebo. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A related lipoprotein marker also decreased modestly. organism: Homo sapiens tissue_or_cell_type: Circulating lipids and lipoproteins experimental_model: Randomized triple-blind placebo-controlled 16-week trial in 120 adults at low-to-moderate cardiovascular risk limitations: Lipid markers rather than cardiovascular events; pantethine is a derivative, not dietary B5 repletion. Absolute changes were small. Industry-associated authors; full methods were not retrieved. exposure: TLC diet begun four weeks before randomization and continued; 60 per group; pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-rumberger2011] Pantethine, a derivative of vitamin B(5) used as a nutritional supplement, favorably alters low-density lipoprotein cholesterol metabolism in low- to moderate-cardiovascular risk North American subjects: a triple-blinded placebo and diet-controlled investigation. (2011). https://pubmed.ncbi.nlm.nih.gov/21925346/ DOI: 10.1016/j.nutres.2011.08.001
Complete structured claim and evidence
The 32-person trial reported LDL-C about 11% below baseline with pantethine at week 16 versus a 3% increase with placebo; the week-16 comparison was significant (P=0.006).
Pantethine → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract; full article retrieval was unavailable.
experimental_model
Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria
exposure
Pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16.
limitations
Small short trial with industry-associated authors and surrogate outcomes; not evidence that pantothenic acid has the same effects or that events or mortality improve. Different effect size from the 2011 trial is not automatically a mechanistic conflict.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The smaller trial also found lower LDL, under its own study conditions.
primary_references
[b5-clin-evans2014] Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation. (2014). https://pubmed.ncbi.nlm.nih.gov/24600231/ DOI: 10.2147/vhrm.s57116
tissue_or_cell_type
Circulating lipids
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1411–1423
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria · source_derived_draft · unverified_draft
### b5-clin-pantethine-ldl-2014 The 32-person trial reported LDL-C about 11% below baseline with pantethine at week 16 versus a 3% increase with placebo; the week-16 comparison was significant (P=0.006). Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The smaller trial also found lower LDL, under its own study conditions. organism: Homo sapiens tissue_or_cell_type: Circulating lipids experimental_model: Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria limitations: Small short trial with industry-associated authors and surrogate outcomes; not evidence that pantothenic acid has the same effects or that events or mortality improve. Different effect size from the 2011 trial is not automatically a mechanistic conflict. exposure: Pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16. cross_nutrient: false evidence_location: Primary indexed abstract; full article retrieval was unavailable. [b5-clin-evans2014] Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation. (2014). https://pubmed.ncbi.nlm.nih.gov/24600231/ DOI: 10.2147/vhrm.s57116
Complete structured claim and evidence
Non-HDL cholesterol differences in the 32-person trial were trends at weeks 8 and 12 and reached significance at week 16 (P=0.042).
Pantethine → Non-HDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract; full article retrieval was unavailable.
experimental_model
Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria
exposure
Pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16.
limitations
Small short trial with industry-associated authors and surrogate outcomes; not evidence that pantothenic acid has the same effects or that events or mortality improve.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The broader non-HDL marker reached statistical significance only at the later measurement.
primary_references
[b5-clin-evans2014] Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation. (2014). https://pubmed.ncbi.nlm.nih.gov/24600231/ DOI: 10.2147/vhrm.s57116
tissue_or_cell_type
Circulating lipids
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1425–1437
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria · source_derived_draft · unverified_draft
### b5-clin-pantethine-nonhdl-2014 Non-HDL cholesterol differences in the 32-person trial were trends at weeks 8 and 12 and reached significance at week 16 (P=0.042). Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The broader non-HDL marker reached statistical significance only at the later measurement. organism: Homo sapiens tissue_or_cell_type: Circulating lipids experimental_model: Randomized triple-blind placebo- and diet-controlled trial in 32 adults eligible for statin therapy under the study criteria limitations: Small short trial with industry-associated authors and surrogate outcomes; not evidence that pantothenic acid has the same effects or that events or mortality improve. exposure: Pantethine 600 mg/day for weeks 1–8 and 900 mg/day for weeks 9–16. cross_nutrient: false evidence_location: Primary indexed abstract; full article retrieval was unavailable. [b5-clin-evans2014] Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation. (2014). https://pubmed.ncbi.nlm.nih.gov/24600231/ DOI: 10.2147/vhrm.s57116
Complete structured claim and evidence
FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115.
Fosmetpantotenate → PKAN activities-of-daily-living score source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Full primary BioC Methods, Results and Discussion.
experimental_model
FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
exposure
24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
limitations
Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The prodrug did not improve the trial’s primary daily-function outcome.
primary_references
[b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
tissue_or_cell_type
Patient/surrogate functional rating and clinician-rated motor performance
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1439–1451
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft
### b5-clin-fort-adl-null FORT found no significant difference in 24-week PKAN-ADL change between fosmetpantotenate and placebo: adjusted difference −0.09 points, 95% CI −1.69 to 1.51, P=0.9115. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The prodrug did not improve the trial’s primary daily-function outcome. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
Complete structured claim and evidence
The secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo.
Fosmetpantotenate → PKAN UPDRS III motor score source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
evidence_location
Full primary BioC Methods, Results and Discussion.
experimental_model
FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants
exposure
24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day.
limitations
Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The clinician-rated motor outcome also failed to show benefit.
primary_references
[b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
tissue_or_cell_type
Patient/surrogate functional rating and clinician-rated motor performance
trigger_kind
machinery_impairment Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1453–1465
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants · source_derived_draft · unverified_draft
### b5-clin-fort-motor-null The secondary UPDRS III motor endpoint also showed no significant treatment difference; mean 24-week changes were +0.7 points with fosmetpantotenate and −1.0 with placebo. Condition category: machinery_impairment nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The clinician-rated motor outcome also failed to show benefit. organism: Homo sapiens tissue_or_cell_type: Patient/surrogate functional rating and clinician-rated motor performance experimental_model: FORT randomized double-blind multicenter placebo-controlled trial; 84 patients aged 6–65 with pathogenic PANK2 variants limitations: Genetic disease, not nutritional B5 deficiency. No measure of brain target engagement was available, so a negative functional endpoint does not locate the failed biochemical step. Sponsor-funded trial; no general safety or dietary-efficacy conclusion. exposure: 24 weeks; fosmetpantotenate 41 versus placebo 43. Adults and children at least 40 kg: 300 mg three times/day; children 20–<40 kg: 150 mg three times/day; children <20 kg: 75 mg three times/day. cross_nutrient: false evidence_location: Full primary BioC Methods, Results and Discussion. [b5-clin-fort2021] Fosmetpantotenate Randomized Controlled Trial in Pantothenate Kinase-Associated Neurodegeneration. (2021). https://pubmed.ncbi.nlm.nih.gov/33200489/ DOI: 10.1002/mds.28392
Complete structured claim and evidence
After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma.
Pantethine → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Pharmacokinetic/metabolic study in four children with nephropathic cystinosis
exposure
Historical oral D-pantethine exposures 70–1000 mg/kg/day.
limitations
Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine.
primary_references
[b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
tissue_or_cell_type
Plasma after oral D-pantethine
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1467–1479
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft
### b5-clin-pantethine-human-products After oral D-pantethine in the four cystinotic children, pantothenic acid and cysteamine appeared as products, while intact pantethine was not detected in plasma. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The administered derivative was rapidly converted; the blood exposure was not simply unchanged pantethine. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. The primary authors described rapid hydrolysis. This human observation does not by itself specify the reductive/disulfide steps or a human vanin isoform. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
Complete structured claim and evidence
Pantothenate after oral pantethine peaked at about 2.5 hours and fitted a two-compartment model with an estimated elimination half-life of 28 hours in the reported cystinosis study.
Pantethine → Blood pantothenate concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract.
experimental_model
Pharmacokinetic/metabolic study in four children with nephropathic cystinosis
exposure
Historical oral D-pantethine exposures 70–1000 mg/kg/day.
limitations
Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. Model-specific estimate at high exposures in four children; not a normal dietary half-life.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Vitamin exposure persisted after the parent derivative was administered.
primary_references
[b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
tissue_or_cell_type
Plasma after oral D-pantethine
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1481–1493
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacokinetic/metabolic study in four children with nephropathic cystinosis · source_derived_draft · unverified_draft
### b5-clin-pantethine-pantothenate-kinetics Pantothenate after oral pantethine peaked at about 2.5 hours and fitted a two-compartment model with an estimated elimination half-life of 28 hours in the reported cystinosis study. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin exposure persisted after the parent derivative was administered. organism: Homo sapiens tissue_or_cell_type: Plasma after oral D-pantethine experimental_model: Pharmacokinetic/metabolic study in four children with nephropathic cystinosis limitations: Very high drug-like exposures in a rare disease; not nutritional dosing, ordinary healthy-person pharmacokinetics or proof of the mechanism behind lipid-trial effects. Rat intestinal-enzyme kinetic data in the same paper are not assigned to humans. Model-specific estimate at high exposures in four children; not a normal dietary half-life. exposure: Historical oral D-pantethine exposures 70–1000 mg/kg/day. cross_nutrient: false evidence_location: Primary indexed abstract. [b5-clin-wittwer1985] Metabolism of pantethine in cystinosis. (1985). https://pubmed.ncbi.nlm.nih.gov/4056044/ DOI: 10.1172/jci112152
Complete structured claim and evidence
Radiolabeled cystine tracing in cystinotic fibroblasts supported formation of cysteamine-cysteine mixed disulfide during pantethine treatment.
Pantethine → Cysteamine-cysteine mixed disulfide source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract, including metabolite-tracing conclusion.
experimental_model
Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts
exposure
Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract.
limitations
Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
The derivative changed accumulated cystine into a different disulfide product in these patient cells.
primary_references
[b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
tissue_or_cell_type
Cystinotic fibroblast lysosomes and extracellular medium
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1495–1507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts · source_derived_draft · unverified_draft
### b5-clin-pantethine-mixed-disulfide Radiolabeled cystine tracing in cystinotic fibroblasts supported formation of cysteamine-cysteine mixed disulfide during pantethine treatment. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The derivative changed accumulated cystine into a different disulfide product in these patient cells. organism: Homo sapiens tissue_or_cell_type: Cystinotic fibroblast lysosomes and extracellular medium experimental_model: Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts limitations: Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis. exposure: Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract. cross_nutrient: false evidence_location: Primary indexed abstract, including metabolite-tracing conclusion. [b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
Complete structured claim and evidence
The cysteamine-cysteine mixed disulfide left treated cystinotic fibroblasts, contributing to depletion of accumulated cellular cystine.
Cysteamine-cysteine mixed disulfide → Cysteamine-cysteine mixed-disulfide efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
false
evidence_location
Primary indexed abstract, including metabolite-tracing conclusion.
experimental_model
Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts
exposure
Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract.
limitations
Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Export of the new disulfide helped remove the stored cystine.
primary_references
[b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
tissue_or_cell_type
Cystinotic fibroblast lysosomes and extracellular medium
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1509–1521
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts · source_derived_draft · unverified_draft
### b5-clin-mixed-disulfide-efflux The cysteamine-cysteine mixed disulfide left treated cystinotic fibroblasts, contributing to depletion of accumulated cellular cystine. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Export of the new disulfide helped remove the stored cystine. organism: Homo sapiens tissue_or_cell_type: Cystinotic fibroblast lysosomes and extracellular medium experimental_model: Radiolabeled cystine metabolite-tracing experiment in cultured patient fibroblasts limitations: Disease-derived cultured cells; no molecular exporter is assigned without evidence. Formation and efflux of a mixed disulfide do not prove that pantothenate alone treats cystinosis. exposure: Pantethine or cystamine treatment; specific concentration not retrieved from the primary abstract. cross_nutrient: false evidence_location: Primary indexed abstract, including metabolite-tracing conclusion. [b5-clin-butler1984] Pantethine and cystamine deplete cystine from cystinotic fibroblasts via efflux of cysteamine-cysteine mixed disulfide. (1984). https://pubmed.ncbi.nlm.nih.gov/6746900/ DOI: 10.1172/jci111436
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Low dietary B5 did not cause a clear increase in intestinal B5 uptake at the tested concentration.

Condition: nutrient_deficiency · Experimental dietary pantothenate restriction in mice; severe deficiency was elicited with antibiotic co-treatment.

Normal role: Intestinal transport supplies pantothenate from the gut to the organism.

Recorded consequence: Dietary pantothenate level did not change mouse intestinal pantothenate uptake assayed at 5 micromolar, including comparisons involving pantothenate-deficient diets.

Scope: Mice fed pantothenic-acid-deficient, normal or high-pantothenic-acid diets; intestinal uptake assays; High, normal and deficient pantothenate diets; uptake assayed at 5 micromolar. An antibiotic was needed to elicit severe deficiency; exact diet amounts and antibiotic are not reported in the abstract.

SMVT supplied most measured pantothenate uptake in the human brain endothelial cell model.

Condition: machinery_impairment · Experimental SLC5A6-specific siRNA knockdown in human brain endothelial cells, used to estimate the transporter contribution to uptake.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: SLC5A6 knockdown analysis attributed 98.6% of total radiolabeled pantothenate uptake to SLC5A6 in human hCMEC/D3 brain endothelial cells.

Scope: Human and monkey brain microvessel analyses; SLC5A6-siRNA experiments in human hCMEC/D3 endothelial cells; SLC5A6-specific siRNA and radiolabeled substrate uptake; tracer concentration not specified in the abstract.

The R123L transporter is largely trapped inside the cell instead of reaching its working surface.

Condition: machinery_impairment · Expression of the SLC5A6 p.Arg123Leu variant.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: Human SLC5A6 R123L-GFP was predominantly retained in the endoplasmic reticulum; ER-marker colocalization supported this localization.

Scope: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants; Live-cell confocal imaging 48 hours after transfection; hSMVT-GFP versus R123L-GFP and DsRed-ER.

The R94X truncation produced little transporter and failed to show normal membrane localization.

Condition: machinery_impairment · Expression of the premature-stop SLC5A6 p.Arg94Ter truncation.

Normal role: SMVT supports cellular availability of pantothenate, biotin and lipoate through shared transport machinery.

Recorded consequence: The truncated SLC5A6 R94X-GFP construct was poorly expressed, with the detected signal localized in the cytoplasm of HuTu-80 and U87 cells.

Scope: Human intestinal HuTu-80 and brain-derived U87 cell transfection and live-cell imaging of patient-derived SLC5A6 variants; Live-cell confocal imaging of equal-DNA transfections under matched imaging settings.

Inherited damage to a B5-using enzyme can cause disease even without low dietary B5.

Condition: machinery_impairment · Inherited or engineered loss of CoA biosynthetic machinery; not dietary pantothenate restriction.

Normal role: CoA biosynthetic enzymes convert pantothenate into usable cellular coenzyme A.

Recorded consequence: The gene-discovery study identified recessive PANK2 defects as the cause of the studied inherited neurodegeneration with brain iron accumulation.

Scope: Human recessive neurodegeneration gene-discovery study; Inherited recessive PANK2 defects; not a controlled vitamin-B5 depletion.

Restoring cysteine can leave a vitamin B5 bottleneck

Condition: nutrient_deficiency · Previously cysteine-depleted Cse-null mice receive cysteine while B5 remains absent.

Normal role: Cells acquire, synthesize and recycle cysteine, then distribute it among protein synthesis, antioxidant systems and sulfur-dependent metabolism.

Recorded consequence: Glutathione recovers more readily than CoA; restoring B5 improves recovery.

Scope: Experimental species, cell type and exposure are retained in every linked record.

This COASY variant disabled the final reaction in the isolated-enzyme test.

Condition: machinery_impairment · Inherited or engineered loss of CoA biosynthetic machinery; not dietary pantothenate restriction.

Normal role: CoA biosynthetic enzymes convert pantothenate into usable cellular coenzyme A.

Recorded consequence: The recombinant COASY DPCK domain carrying p.Arg499Cys did not produce a detectable CoA HPLC peak, whereas wild-type DPCK converted dephospho-CoA to CoA.

Scope: Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies; HPLC assays with 1 microgram recombinant wild-type or p.Arg499Cys DPCK protein, ATP and dephospho-CoA; substrate concentrations not extracted.

A severe enzyme defect did not imply an absent whole-cell free-CoA pool in these fibroblasts.

Condition: machinery_impairment · Inherited or engineered loss of CoA biosynthetic machinery; not dietary pantothenate restriction.

Normal role: CoA biosynthetic enzymes convert pantothenate into usable cellular coenzyme A.

Recorded consequence: Free-CoA levels in fibroblasts from the two COASY cases were not significantly different from the control in the reported HPLC analysis.

Scope: Two unrelated human NBIA cases, primary fibroblasts, recombinant wild-type and variant COASY DPCK domains and yeast studies; Two affected individuals versus one healthy-control fibroblast line; four independent experiments shown in Fig. 6.

A downstream intermediate improved a mitochondrial enzyme measurement in this genetic mouse model.

Condition: machinery_impairment · Inherited or engineered loss of CoA biosynthetic machinery; not dietary pantothenate restriction.

Normal role: CoA biosynthetic enzymes convert pantothenate into usable cellular coenzyme A.

Recorded consequence: Oral 4′-phosphopantetheine corrected the complex I activity defect in globus-pallidus-enriched brain tissue from Pank2-null mice.

Scope: C57/BL6 Pank2-null mice, both sexes aged 3–6 months, with globus-pallidus-enriched brain dissection; human PKAN cell experiments; Oral 4′-phosphopantetheine in 10% sucrose for 14 days; efficacy regimen 5 micrograms/g body weight (5 mg/kg); both-sex Pank2-null C57/BL6 mice aged 3–6 months; Fig. 2E n=5 per genotype/treatment group.

Loss of the mitochondrial carrier impaired attachment of the lipoate cofactor to proteins.

Condition: machinery_impairment · ACP mRNA and protein reduced by more than 85% within 24 hours; later measurements followed knockdown.