Component
Mouse Kdm2a / Jhdm1a
Murine JmjC histone lysine demethylase Kdm2a.
2 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.
Where it participates (unsigned role)
Vitamin C treatment reduced H3K36me2/3 in mouse embryonic fibroblasts during culture and reprogramming, linking the intervention to histone methylation changes.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary abstract H3K36me2/3 result
- experimental_model
- Mouse embryonic fibroblasts in culture and reprogramming; primary abstract-level result
- exposure
- Vitamin C-supplemented cell culture; exact preparation, dose and duration not recovered from accessible primary abstract.
- limitations
- No direct claim that Kdm2a/b remove H3K36me3; the combined cellular mark change may involve other enzymes. Abstract-only exposure resolution.
- 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 changed methyl marks on histone proteins in cultured mouse fibroblasts.
- primary_references
- [c-reg-wang] The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin-C-dependent manner. (2011). https://pubmed.ncbi.nlm.nih.gov/22100412/ DOI: 10.1016/j.stem.2011.10.005
- tissue_or_cell_type
- Embryonic fibroblasts
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1089–1101
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse embryonic fibroblasts in culture and reprogramming; primary abstract-level result · source_derived_draft · unverified_draft
### c-reg-h3k36-mark-reduction Vitamin C treatment reduced H3K36me2/3 in mouse embryonic fibroblasts during culture and reprogramming, linking the intervention to histone methylation changes. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C changed methyl marks on histone proteins in cultured mouse fibroblasts. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: Mouse embryonic fibroblasts in culture and reprogramming; primary abstract-level result limitations: No direct claim that Kdm2a/b remove H3K36me3; the combined cellular mark change may involve other enzymes. Abstract-only exposure resolution. exposure: Vitamin C-supplemented cell culture; exact preparation, dose and duration not recovered from accessible primary abstract. cross_nutrient: false evidence_location: Primary abstract H3K36me2/3 result [c-reg-wang] The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin-C-dependent manner. (2011). https://pubmed.ncbi.nlm.nih.gov/22100412/ DOI: 10.1016/j.stem.2011.10.005
Complete structured claim and evidenceJhdm1a/1b gain- and loss-of-function experiments identified these histone demethylases as functional effectors of vitamin-C-enhanced mouse somatic-cell reprogramming. Loss-of-function reduced the response rather than being corrected by vitamin C alone.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Primary abstract gain/loss-of-function result
- experimental_model
- Mouse fibroblast reprogramming with Jhdm1a/1b gain/loss of function
- exposure
- Genetic gain/loss interventions during vitamin C-supported reprogramming; exact construct, dose and timing not recovered.
- limitations
- Abstract-level mechanistic assignment; no quantitative effect size or specific knockdown efficiency asserted.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Mus musculus
- plain_language
- The histone enzymes were part of the machinery through which vitamin C helped cells reprogram.
- primary_references
- [c-reg-wang] The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin-C-dependent manner. (2011). https://pubmed.ncbi.nlm.nih.gov/22100412/ DOI: 10.1016/j.stem.2011.10.005
- tissue_or_cell_type
- Embryonic fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1103–1115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse fibroblast reprogramming with Jhdm1a/1b gain/loss of function · source_derived_draft · unverified_draft
### c-reg-jhdm-reprogramming-effectors Jhdm1a/1b gain- and loss-of-function experiments identified these histone demethylases as functional effectors of vitamin-C-enhanced mouse somatic-cell reprogramming. Loss-of-function reduced the response rather than being corrected by vitamin C alone. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: The histone enzymes were part of the machinery through which vitamin C helped cells reprogram. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: Mouse fibroblast reprogramming with Jhdm1a/1b gain/loss of function limitations: Abstract-level mechanistic assignment; no quantitative effect size or specific knockdown efficiency asserted. exposure: Genetic gain/loss interventions during vitamin C-supported reprogramming; exact construct, dose and timing not recovered. cross_nutrient: false evidence_location: Primary abstract gain/loss-of-function result [c-reg-wang] The histone demethylases Jhdm1a/1b enhance somatic cell reprogramming in a vitamin-C-dependent manner. (2011). https://pubmed.ncbi.nlm.nih.gov/22100412/ DOI: 10.1016/j.stem.2011.10.005
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.