Component

Mouse ATP-citrate lyase / Acly

Mouse ATP-citrate lyase / Acly. Identity is distinct from its gene and experimentally modified states; see each claim for organism and scope.

1 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.

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

Where it participates (unsigned role)

  1. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards