Component
TET1
Human ten-eleven translocation methylcytosine dioxygenase 1; human catalytic domain used by Blaschke et al.
3 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 it acts on
TET1 knockdown reduced luteolin-associated sub-G1 accumulation and nuclear fragmentation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Human colon cancer siRNA experiment.
- limitations
- No clinical efficacy or nutrient-supplement rescue established.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Removing machinery weakened the observed cell-death response.
- primary_references
- Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 492–498
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colon cancer siRNA experiment. · source_derived_draft · unverified_draft
## luteolin-tet1-knockdown Removing machinery weakened the observed cell-death response. TET1 knockdown reduced luteolin-associated sub-G1 accumulation and nuclear fragmentation. Model: Human colon cancer siRNA experiment. Limitations: No clinical efficacy or nutrient-supplement rescue established. Evidence access: Primary full text Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y
Complete structured claim and evidence
What acts on it
Luteolin increased TET1 association with the NFE2L2 promoter in human colon cancer cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human cell ChIP; 10–60 micromolar studies.
- limitations
- Promoter association is not a direct luteolin–TET1 binding assay.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- DNA-modifying machinery participates in the response.
- primary_references
- Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 484–490
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cell ChIP; 10–60 micromolar studies. · source_derived_draft · unverified_draft
## luteolin-tet1-recruitment DNA-modifying machinery participates in the response. Luteolin increased TET1 association with the NFE2L2 promoter in human colon cancer cells. Model: Human cell ChIP; 10–60 micromolar studies. Limitations: Promoter association is not a direct luteolin–TET1 binding assay. Evidence access: Primary full text Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30988303/ · DOI 10.1038/s12276-019-0238-y
Complete structured claim and evidenceVitamin C increased hydroxymethylcytosine production by recombinant human TET1 catalytic domain in the reported pH 8.0 assay containing Fe(II) and 2-oxoglutarate. This demonstrates assay enhancement, without establishing obligatory ascorbate binding.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Figure 3a; Methods Tet activity assay
- experimental_model
- Purified recombinant human TET1 catalytic-domain assay; antibody detection of hydroxymethylated biotinylated DNA
- exposure
- 10 min at 37°C; 1.2 µg enzyme, 178.2 ng DNA, 3.7 µM ammonium iron(II) sulfate, 1 mM 2-oxoglutarate, titrated vitamin C (Sigma A5960).
- limitations
- Purified-domain result; oxidation-prone buffer differs from cellular iron conditions. Exact plotted titration values not transcribed.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Homo sapiens protein
- plain_language
- Vitamin C helped the isolated human enzyme modify DNA under these test conditions.
- primary_references
- [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
- tissue_or_cell_type
- Cell-free
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 963–975
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human TET1 catalytic-domain assay; antibody detection of hydroxymethylated biotinylated DNA · source_derived_draft · unverified_draft
### c-reg-tet1-human-activity Vitamin C increased hydroxymethylcytosine production by recombinant human TET1 catalytic domain in the reported pH 8.0 assay containing Fe(II) and 2-oxoglutarate. This demonstrates assay enhancement, without establishing obligatory ascorbate binding. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C helped the isolated human enzyme modify DNA under these test conditions. organism: Homo sapiens protein tissue_or_cell_type: Cell-free experimental_model: Purified recombinant human TET1 catalytic-domain assay; antibody detection of hydroxymethylated biotinylated DNA limitations: Purified-domain result; oxidation-prone buffer differs from cellular iron conditions. Exact plotted titration values not transcribed. exposure: 10 min at 37°C; 1.2 µg enzyme, 178.2 ng DNA, 3.7 µM ammonium iron(II) sulfate, 1 mM 2-oxoglutarate, titrated vitamin C (Sigma A5960). cross_nutrient: true evidence_location: Figure 3a; Methods Tet activity assay [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
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.