Component

Mitochondrial acetyl-CoA synthetase 1 / ACSS1

Mitochondrial acetyl-CoA synthetase 1 / ACSS1. Species, exposure and limitations are retained in each linked claim.

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. Exogenous acetate uptake is controlled by expression of both ACSS2 and the mitochondrial ACSS1, and the mitochondrial and lipogenic demand for two-carbon acetyl units considerably exceeds the uptake of exogenous acetate, leaving it to only sparingly contribute to histone acetylation.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"}
    experimental_model
    Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation
    exposure
    Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation
    limitations
    The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Cultured cells
    plain_language
    Acetate taken in from outside is mostly burned or built into fat; very little of it reaches the histones.
    primary_references
    [acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055
    tissue_or_cell_type
    Nucleus and cytosol

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 589–600

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation · source_derived_draft · unverified_draft

    ### acetate-exogenous-acetate-sparing Exogenous acetate uptake is controlled by expression of both ACSS2 and the mitochondrial ACSS1, and the mitochondrial and lipogenic demand for two-carbon acetyl units considerably exceeds the uptake of exogenous acetate, leaving it to only sparingly contribute to histone acetylation. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Acetate taken in from outside is mostly burned or built into fat; very little of it reaches the histones. organism: Cultured cells tissue_or_cell_type: Nucleus and cytosol experimental_model: Quantitative analysis of acetate metabolism in cultured cells under oxygen and serum limitation limitations: The quantitative accounting here is the important part and it is a limiting result: demand for two-carbon units far exceeds what exogenous acetate supplies. Cultured cells at a given acetate concentration, which is not a fed human. exposure: Exogenous acetate with ACSS2 and ACSS1 manipulation under oxygen and serum limitation evidence_span: {"source_cache": "artifacts/acetate-research/28099844.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188", "start_char": 0, "end_char": 1134, "text_sha256": "6df5e8ccde04ad8a222db774f6a8b1e8838ad6a1d918ff84b667d6dde57de188"} [acetate-p28099844] Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation. (2017). https://pubmed.ncbi.nlm.nih.gov/28099844/ DOI: 10.1016/j.celrep.2016.12.055
    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