Component
Mouse Tet2 gene
Mus musculus Tet2 gene; genotype and expression interventions specified per claim.
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
Deleting a 104-bp intronic segment encompassing the mouse Tet2 retinoic-acid response element prevented the normal retinol-dependent Tet2 mRNA increase, supporting a cis-regulatory requirement.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Figure 3E–F
- experimental_model
- CRISPR Tet2 ΔRARE naïve ESCs compared with wild type
- exposure
- Retinol titration as in Figure 3F; 104-bp deletion NCBI37 chr3:133197151–133197253.
- limitations
- Deletion tests the segment rather than one isolated nucleotide; this is engineered machinery impairment, not vitamin A deficiency.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Mus musculus
- plain_language
- The vitamin A response depended on a specific DNA control sequence in the Tet2 gene.
- primary_references
- [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
- tissue_or_cell_type
- Naïve embryonic stem cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1061–1073
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR Tet2 ΔRARE naïve ESCs compared with wild type · source_derived_draft · unverified_draft
### c-reg-tet2-rare-deletion Deleting a 104-bp intronic segment encompassing the mouse Tet2 retinoic-acid response element prevented the normal retinol-dependent Tet2 mRNA increase, supporting a cis-regulatory requirement. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: The vitamin A response depended on a specific DNA control sequence in the Tet2 gene. organism: Mus musculus tissue_or_cell_type: Naïve embryonic stem cells experimental_model: CRISPR Tet2 ΔRARE naïve ESCs compared with wild type limitations: Deletion tests the segment rather than one isolated nucleotide; this is engineered machinery impairment, not vitamin A deficiency. exposure: Retinol titration as in Figure 3F; 104-bp deletion NCBI37 chr3:133197151–133197253. cross_nutrient: true evidence_location: Figure 3E–F [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
Complete structured claim and evidence
What acts on it
Retinol supplementation increased Tet2 transcription in mouse naïve ESCs within 8 h and after 72 h; Tet3 also responded, whereas evidence did not support direct retinol stimulation of TET catalytic efficiency.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Figure 3A–C
- experimental_model
- Mouse naïve ESCs in vitamin-A-free N2B27/2i medium; transcript quantification
- exposure
- Retinol titration 0–50 ng/mL; 8-h and 72-h transcript assays.
- limitations
- Retinoid signaling and response depend on culture context; no claim that vitamin A supplementation demethylates adult human tissues.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Mus musculus
- plain_language
- Vitamin A raised expression of DNA-modifying enzymes through a different route from vitamin C’s iron-redox effect.
- primary_references
- [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
- tissue_or_cell_type
- Naïve embryonic stem cells
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1047–1059
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse naïve ESCs in vitamin-A-free N2B27/2i medium; transcript quantification · source_derived_draft · unverified_draft
### c-reg-retinol-tet2-expression Retinol supplementation increased Tet2 transcription in mouse naïve ESCs within 8 h and after 72 h; Tet3 also responded, whereas evidence did not support direct retinol stimulation of TET catalytic efficiency. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A raised expression of DNA-modifying enzymes through a different route from vitamin C’s iron-redox effect. organism: Mus musculus tissue_or_cell_type: Naïve embryonic stem cells experimental_model: Mouse naïve ESCs in vitamin-A-free N2B27/2i medium; transcript quantification limitations: Retinoid signaling and response depend on culture context; no claim that vitamin A supplementation demethylates adult human tissues. exposure: Retinol titration 0–50 ng/mL; 8-h and 72-h transcript assays. cross_nutrient: true evidence_location: Figure 3A–C [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113
Complete structured claim and evidence
Where it participates (unsigned role)
Combined Tet1/Tet2 deletion in mouse ESCs abolished the vitamin-C-induced increase in 5hmC and promoter demethylation observed in wild-type cells; residual antibody signal was not interpreted as robust Tet activity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Figure 3b–c
- experimental_model
- Tet1/Tet2 double-knockout ESCs versus wild type; dot blot and DIP-qPCR
- exposure
- 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
- limitations
- Genetic loss of machinery, not low vitamin intake; other vitamin C effects and residual Tet3 were not excluded.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Mus musculus
- plain_language
- Vitamin C could not restore these DNA effects when the two relevant enzymes were genetically absent.
- 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
- Embryonic stem cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1005–1017
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tet1/Tet2 double-knockout ESCs versus wild type; dot blot and DIP-qPCR · source_derived_draft · unverified_draft
### c-reg-tet-dko-blocks-response Combined Tet1/Tet2 deletion in mouse ESCs abolished the vitamin-C-induced increase in 5hmC and promoter demethylation observed in wild-type cells; residual antibody signal was not interpreted as robust Tet activity. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C could not restore these DNA effects when the two relevant enzymes were genetically absent. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Tet1/Tet2 double-knockout ESCs versus wild type; dot blot and DIP-qPCR limitations: Genetic loss of machinery, not low vitamin intake; other vitamin C effects and residual Tet3 were not excluded. exposure: 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling. cross_nutrient: false evidence_location: Figure 3b–c [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.