ArticleEpigenetics & chromatin2025
Loss of TET2 activity limits the ability of vitamin C to activate DNA demethylation in human HAP1 cells.
Article in Epigenetics & chromatin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- TET Enzymes as Epigenetic Integrators in Intestinal Immunity, Inflammation, and Disease.Journal of personalized medicine · 2026Review
- Mechanisms and therapeutic prospects of DNA methylation-mucosal innate immunity crosstalk in inflammatory bowel disease.Frontiers in immunology · 2026Review
- Increased phenotypic and functional stability of human allospecific induced Tregs is associated with Vitamin C-mediatedFrontiers in immunology · 2026Article
- TET2 downregulation limits oxidative stress-induced cytotoxicity of high dose ascorbate in dabrafenib-resistant melanoma cells.Cancer drug resistance (Alhambra, Calif.) · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundThe TET family of proteins-TET1, TET2, and TET3-are α-KG and Fe
resultsOur findings reveal that TET2 is essential for all steps of iterative oxidation, and its loss has the most significant effect on 5-hydroxymethylcytosine and 5-formylcytosine levels. Vitamin C enhances TET activity and increases the levels of these oxidation products. However, its effect in TET2 knockout cells is limited. Vitamin C increased cytosine modification levels in TET2KO cells, but not to the extent observed in treated wild-type cells, indicating incomplete compensation for TET2 loss.
conclusionsOur results demonstrated that each TET protein has a distinct, separate contribution to generating active demethylation products. The absence of individual TET paralog is linked with the specific pattern of active demethylation products in DNA, which is preserved after vitamin C treatment. Therefore, the deletion of one of the TET enzymes cannot be compensated for by the increased activity of the other TET family members, highlighting the unique roles of each TET paralog in epigenetic regulation.
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