Component
Human cancer-cell RAD51 repair foci
Human cancer-cell RAD51 repair foci
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.
What acts on it
ALCAR restored impaired RAD51-foci responses under IDH1-inhibited DNA-repair conditions.
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": "ALCAR plus IDH1 inhibition", "comparator": "IDH1 inhibition without ALCAR", "endpoint": "ALCAR restored impaired RAD51-foci responses under IDH1-inhibited DNA-repair conditions.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Human U2OS inducible double-strand-break system; Fig. 4h. Methods: ALCAR 1 mM, GSK864 10 micromolar for five days before induced breaks.
- 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 impaired RAD51-foci responses under IDH1-inhibited DNA-repair conditions.
- 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-rad51-rescue; RAD51 recruitment is a repair readout, not proof that ALCAR prevents cancer or that a dietary dose changes tumor survival.
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 344–350
AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Human U2OS inducible double-strand-break system; Fig. 4h. Methods: ALCAR 1 mM, GSK864 10 micromolar for five days before induced breaks. · Recorded from source · Recorded from source
### cancer-rad51-rescue ALCAR restored impaired RAD51-foci responses under IDH1-inhibited DNA-repair conditions. RAD51 recruitment is a repair readout, not proof that ALCAR prevents cancer or that a dietary dose changes tumor survival. Model and exposure: Human U2OS inducible double-strand-break system; Fig. 4h. Methods: ALCAR 1 mM, GSK864 10 micromolar for five days before induced breaks. 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
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.