Component
Cytosine oxidation products in human HAP1 TET-knockout cells
5-hydroxymethylcytosine and 5-formylcytosine measured by 2D-UPLC-MS/MS.
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
TET2 knockout in human HAP1 cells lowered 5-hydroxymethylcytosine and 5-formylcytosine measured by 2D-UPLC-MS/MS, and vitamin C treatment did not restore them to the levels seen in treated wild-type cells, so loss of one TET paralog was not compensated by the remaining ones.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- duration
- Culture experiments
- experimental_model
- Human HAP1 cells with single and double TET knockouts
- exposure
- Vitamin C treatment of wild-type and TET-knockout cells
- limitations
- A near-haploid cell line, not a haematopoietic cell; a knockout is not a patient's point mutation.
- organism
- Homo sapiens
- plain_language
- Vitamin C cannot fully substitute for a TET2 that is missing.
- primary_references
- [kusmierek-2025] Loss of TET2 activity limits the ability of vitamin C to activate DNA demethylation in human HAP1 cells (2025). https://pubmed.ncbi.nlm.nih.gov/41287077/ DOI: 10.1186/s13072-025-00634-1
- tissue
- HAP1 cell line
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
TET2 loss and malignancy: the step between a nutrient-responsive enzyme and the disease (2026-09-23) · lines 183–191
Original AI-assisted curation of twelve primary studies located by Europe PMC title search, with every statement drafted from the retrieved abstract. Two pairs share a laboratory and are recorded as one line of evidence each. Genetic loss of function, pharmacological exposure and dietary depletion are kept as separate record types. Not publisher full text. · supports · Human HAP1 cells with single and double TET knockouts · source_derived_draft · unverified_draft
## vitamin-c-cannot-replace-lost-tet2 TET2 knockout in human HAP1 cells lowered 5-hydroxymethylcytosine and 5-formylcytosine measured by 2D-UPLC-MS/MS, and vitamin C treatment did not restore them to the levels seen in treated wild-type cells, so loss of one TET paralog was not compensated by the remaining ones. Model/species: Human HAP1 cells with single and double TET knockouts Organism: Homo sapiens Tissue/system: HAP1 cell line Exposure: Vitamin C treatment of wild-type and TET-knockout cells Duration: Culture experiments Limits: A near-haploid cell line, not a haematopoietic cell; a knockout is not a patient's point mutation. Primary reference: [kusmierek-2025] Loss of TET2 activity limits the ability of vitamin C to activate DNA demethylation in human HAP1 cells (2025). https://pubmed.ncbi.nlm.nih.gov/41287077/ DOI: 10.1186/s13072-025-00634-1
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.