Component
Histone acetyltransferase activity
Histone acetyltransferase activity. 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.
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.
Where it participates (unsigned role)
Acetate supplementation had no effect on histone acetyltransferase activity in brain extracts but significantly inhibited histone deacetylase activity twofold at 2 and 4 hours after treatment and decreased HDAC 2 levels at 4 hours, leading the authors to conclude that acetyl-CoA derived from acetate supplementation increases brain histone acetylation state by reducing deacetylase activity and expression.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/acetate-research/21359531.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b", "start_char": 0, "end_char": 1456, "text_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b"}
- experimental_model
- Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose
- exposure
- A single oral dose of 6 g/kg glyceryl triacetate, an acetate precursor
- limitations
- A large single dose of a precursor, not dietary acetate. The mechanism is loss of deacetylation rather than added acetylation, and only some marks moved.
- 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
- Rat
- plain_language
- The marks accumulated because they were being removed more slowly, not because more were being added.
- primary_references
- [acetate-p21359531] Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression. (2011). https://pubmed.ncbi.nlm.nih.gov/21359531/ DOI: 10.1007/s11010-011-0751-3
- tissue_or_cell_type
- Brain and liver
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 667–678
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose · source_derived_draft · unverified_draft
### acetate-acetate-inhibits-hdac Acetate supplementation had no effect on histone acetyltransferase activity in brain extracts but significantly inhibited histone deacetylase activity twofold at 2 and 4 hours after treatment and decreased HDAC 2 levels at 4 hours, leading the authors to conclude that acetyl-CoA derived from acetate supplementation increases brain histone acetylation state by reducing deacetylase activity and expression. 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: The marks accumulated because they were being removed more slowly, not because more were being added. organism: Rat tissue_or_cell_type: Brain and liver experimental_model: Time-course Western blot analysis of brain and liver histone acetylation in rats after a single oral dose limitations: A large single dose of a precursor, not dietary acetate. The mechanism is loss of deacetylation rather than added acetylation, and only some marks moved. exposure: A single oral dose of 6 g/kg glyceryl triacetate, an acetate precursor evidence_span: {"source_cache": "artifacts/acetate-research/21359531.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b", "start_char": 0, "end_char": 1456, "text_sha256": "a60e30b6fa78f5fc4d9da17279ec1ecc29dd20939df5771ba26996900102014b"} [acetate-p21359531] Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression. (2011). https://pubmed.ncbi.nlm.nih.gov/21359531/ DOI: 10.1007/s11010-011-0751-3
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.