Component

4′-Phosphopantetheine

4′-Phosphopantetheine. See linked evidence for experiment-specific scope. 4′-Phosphopantetheine. Identity is distinct from its gene and experimentally modified states; see each claim for organism and scope.

16 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. 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

  2. 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

What acts on it

  1. 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

  2. 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

Where it participates (unsigned role)

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

In the sources

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