Component

Human cancer-cell histone acetylation

Human cancer-cell histone acetylation

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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 restored histone acetylation after CRAT knockdown, whereas L-carnitine did not, in the 2026 cancer models.

    Acetyl-L-carnitine → Human cancer-cell histone acetylation Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_condition
    CRAT-knockdown cells without ALCAR knocked down · Human carnitine acetyltransferase / CRAT Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    CRAT-knockdown cells without ALCAR supplied · Acetyl-L-carnitine Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "ALCAR added after CRAT knockdown", "comparator": "CRAT-knockdown cells without ALCAR", "endpoint": "ALCAR restored histone acetylation after CRAT knockdown, whereas L-carnitine did not, in the 2026 cancer models.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "acetylcarnitine", "state": "supplied"}, {"entity_slug": "human-crat", "state": "knocked down"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human cancer-cell CRAT knockdown; Extended Data Fig. 6c.
    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 restored histone acetylation after CRAT knockdown, whereas L-carnitine did not, in the 2026 cancer models.
    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-crat-bypass; Supplying the acetylated product bypassed this perturbation under the tested conditions. The result does not establish a neuron-wide pathway.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 296–302

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human cancer-cell CRAT knockdown; Extended Data Fig. 6c. · Recorded from source · Recorded from source

    ### cancer-crat-bypass ALCAR restored histone acetylation after CRAT knockdown, whereas L-carnitine did not, in the 2026 cancer models. Supplying the acetylated product bypassed this perturbation under the tested conditions. The result does not establish a neuron-wide pathway. Model and exposure: Human cancer-cell CRAT knockdown; Extended Data Fig. 6c. 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

  2. ALCAR failed to restore histone acetylation after CROT knockdown in the 2026 cancer models.

    Acetyl-L-carnitine → Human cancer-cell histone acetylation Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_condition
    CROT-knockdown cells without added ALCAR supplied · Acetyl-L-carnitine Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    CROT-knockdown cells without added ALCAR knocked down · Human carnitine octanoyltransferase / CROT Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "ALCAR added after CROT knockdown", "comparator": "CROT-knockdown cells without added ALCAR", "endpoint": "ALCAR failed to restore histone acetylation after CROT knockdown in the 2026 cancer models.", "effect_direction": "no_detected_change", "combination": "joint", "conditions": [{"entity_slug": "acetylcarnitine", "state": "supplied"}, {"entity_slug": "human-crot", "state": "knocked down"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human cancer-cell CROT knockdown; Extended Data Fig. 6d.
    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 failed to restore histone acetylation after CROT knockdown in the 2026 cancer models.
    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-crot-no-bypass; The result implicates CROT-dependent processing in this setting; it does not mean that CROT is the only enzyme capable of using ALCAR in all tissues.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 304–310

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human cancer-cell CROT knockdown; Extended Data Fig. 6d. · Recorded from source · Recorded from source

    ### cancer-crot-no-bypass ALCAR failed to restore histone acetylation after CROT knockdown in the 2026 cancer models. The result implicates CROT-dependent processing in this setting; it does not mean that CROT is the only enzyme capable of using ALCAR in all tissues. Model and exposure: Human cancer-cell CROT knockdown; Extended Data Fig. 6d. 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

  3. TMLHE knockdown reduced histone acetylation and nuclear acetyl-CoA in the 2026 cancer-cell study.

    Trimethyllysine hydroxylase / TMLHE → Human cancer-cell histone acetylation Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "TMLHE knockdown", "comparator": "Control shRNA", "endpoint": "TMLHE knockdown reduced histone acetylation and nuclear acetyl-CoA in the 2026 cancer-cell study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human FT282-CCNE1 and Ovcar8-CCNE1 models; Fig. 3g,j.
    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
    TMLHE knockdown reduced histone acetylation and nuclear acetyl-CoA 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 tmlhe-histone-loss; L-carnitine or ALCAR rescued acetylation downstream of TMLHE loss; alpha-ketoglutarate did not. This distinguishes a blocked enzyme step from insufficient upstream cosubstrate.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 288–294

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human FT282-CCNE1 and Ovcar8-CCNE1 models; Fig. 3g,j. · Recorded from source · Recorded from source

    ### tmlhe-histone-loss TMLHE knockdown reduced histone acetylation and nuclear acetyl-CoA in the 2026 cancer-cell study. L-carnitine or ALCAR rescued acetylation downstream of TMLHE loss; alpha-ketoglutarate did not. This distinguishes a blocked enzyme step from insufficient upstream cosubstrate. Model and exposure: Human FT282-CCNE1 and Ovcar8-CCNE1 models; Fig. 3g,j. 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.