Component
Cellular de novo coenzyme A synthesis
Cellular de novo coenzyme A synthesis. See linked evidence for experiment-specific 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
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.
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
Where it participates (unsigned role)
AKT phosphorylation of PANK4 relieved its suppression of de novo CoA synthesis in the study models.
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
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.