Component
Human phosphopantetheinylated mitochondrial ACP
Human phosphopantetheinylated mitochondrial ACP. Identity is distinct from its gene and experimentally modified states; see each claim for organism and scope.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Human AASDHPPT transfers the CoA-derived 4′-phosphopantetheine group to a conserved serine in human mitochondrial ACP.
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
Where it participates (unsigned role)
Mitochondrial ACP knockdown in HEK293T cells subsequently reduced respiratory complex I specific activity.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.