Component
L-Ascorbic acid 2-phosphate
Stable phosphorylated vitamin C derivative used in cell culture; distinguish from unmodified ascorbate.
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
Adding L-ascorbic acid 2-phosphate to mouse ESC medium rapidly increased global DNA 5hmC and promoter-associated 5hmC, preceding later methylcytosine loss.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Figures 1–2
- experimental_model
- Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation
- exposure
- 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
- limitations
- 5hmC abundance alone is not proof of completed demethylation; cultured ESCs are not 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
- A stable vitamin C derivative increased an early DNA-demethylation intermediate in cultured mouse stem cells.
- 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
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 977–989
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation · source_derived_draft · unverified_draft
### c-reg-esc-hydroxymethylation Adding L-ascorbic acid 2-phosphate to mouse ESC medium rapidly increased global DNA 5hmC and promoter-associated 5hmC, preceding later methylcytosine loss. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: A stable vitamin C derivative increased an early DNA-demethylation intermediate in cultured mouse stem cells. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation limitations: 5hmC abundance alone is not proof of completed demethylation; cultured ESCs are not adult human tissues. exposure: 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling. cross_nutrient: false evidence_location: Figures 1–2 [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 evidenceAfter vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Figure 2; resistant-region analysis
- experimental_model
- Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation
- exposure
- 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
- limitations
- Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene.
- 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 selected DNA methylation patterns in these cells; protected regions retained their marks.
- 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
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 991–1003
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation · source_derived_draft · unverified_draft
### c-reg-esc-promoter-demethylation After vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C changed selected DNA methylation patterns in these cells; protected regions retained their marks. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation limitations: Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene. 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 2; resistant-region analysis [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
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.