Component

Human cancer-cell H3K23/H4K8/H4K12 acetyl carbon

Human cancer-cell H3K23/H4K8/H4K12 acetyl carbon

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

What acts on it

  1. ALCAR acetyl carbon was traced into H3K23ac, H4K8ac and H4K12ac in the 2026 cancer-cell study.

    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_model
    Stable-isotope tracing, Extended Data Fig. 8e; site-specific histone mass spectrometry.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    ALCAR acetyl carbon was traced into H3K23ac, H4K8ac and H4K12ac in the 2026 cancer-cell study.
    primary_references
    αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7
    source_locator
    Reviewed reference cancer-histone-sites; These marks were sensitive to the alpha-ketoglutarate/TMLHE/carnitine axis. They are not the same promoter-specific H3K27 readout measured in the rat depression study.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 320–326

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Stable-isotope tracing, Extended Data Fig. 8e; site-specific histone mass spectrometry. · Recorded from source · Recorded from source

    ### cancer-histone-sites ALCAR acetyl carbon was traced into H3K23ac, H4K8ac and H4K12ac in the 2026 cancer-cell study. These marks were sensitive to the alpha-ketoglutarate/TMLHE/carnitine axis. They are not the same promoter-specific H3K27 readout measured in the rat depression study. Model and exposure: Stable-isotope tracing, Extended Data Fig. 8e; site-specific histone mass spectrometry. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | 2026 | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.