ArticleThe Journal of biological chemistry2020
14-3-3 proteins protect AMPK-phosphorylated ten-eleven translocation-2 (TET2) from PP2A-mediated dephosphorylation.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Genomic sequence context differentially impacts stepwise oxidation by TET enzymes to shape DNA hydroxymethylation landscapes.Nucleic acids research · 2026Article
- B cell TET2 recruits OGT for nuclear TET2 and H2B O-GlcNAcylation to drive AID and BLIMP-1 expression and maturation of the antibody response.Cell reports · 2026Article
- TET2 in epigenetic control of immune cells: Implications for inflammatory responses and age-related pathologies.The Journal of biological chemistry · 2026Review
- Apoptotic bodies derived from human umbilical cord mesenchymal stem cells improve recovery from myocardial infarction in swine.Autophagy · 2026Article
- The role of calcium homeostasis dysregulation in allergic rhinitis.Frontiers in immunology · 2026Review
- Clonal Hematopoiesis of Indeterminate Potential and Cardiometabolic Disease: Challenges, Controversies and Future Perspectives.International journal of molecular sciences · 2025Review
- Genetic adaptations shaping survival, pregnancy, and life at high altitude and sea level.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Increased iron uptake by splenic hematopoietic stem cells promotes TET2-dependent erythroid regeneration.Nature communications · 2024Article
- The Integration of Proteome-Wide PTM Data with Protein Structural and Sequence Features Identifies Phosphorylations that Mediate 14-3-3 Interactions.Journal of molecular biology · 2023Article
- Research progress of AMP-activated protein kinase and cardiac aging.Open life sciences · 2023Review
- Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022Review
- Small Heat Shock Protein 22 Improves Cognition and Learning in the Tauopathic Brain.International journal of molecular sciences · 2022Article
- Research progress on the relationship between the TOR signaling pathway regulator, epigenetics, and tumor development.Frontiers in genetics · 2022Review
- DysregulatedCancers · 2021Review
- The TGF-β/HDAC7 axis suppresses TCA cycle metabolism in renal cancer.JCI insight · 2021Article
- AMPK: restoring metabolic homeostasis over space and time.Molecular cell · 2021Review
- The function and regulation of TET2 in innate immunity and inflammation.Protein & cell · 2021Review
- The Role of Host Cell DNA Methylation in the Immune Response to Bacterial Infection.Frontiers in immunology · 2021Review
- TET-dioxygenase deficiency in oncogenesis and its targeting for tumor-selective therapeutics.Seminars in hematology · 2021Review
- USP15 suppresses tumor immunity via deubiquitylation and inactivation of TET2.Science advances · 2020Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Ten-eleven translocation-2 (TET2) is a member of the methylcytosine dioxygenase family of enzymes and has been implicated in cancer and aging because of its role as a global epigenetic modifier. TET2 has a large N-terminal domain and a catalytic C-terminal region. Previous reports have demonstrated that the TET2 catalytic domain remains active independently of the N-terminal domain. As such, the function of the N terminus of this large protein remains poorly characterized. Here, using yeast two-hybrid screening, co-immunoprecipitation, and several biochemical assays, we found that several isoforms of the 14-3-3 family of proteins bind TET2. 14-3-3 proteins bound TET2 when it was phosphorylated at Ser-99. In particular, we observed that AMP-activated protein kinase-mediated phosphorylation at Ser-99 promotes TET2 stability and increases global DNA 5-hydroxymethylcytosine levels. The interaction of 14-3-3 proteins with TET2 protected the Ser-99 phosphorylation, and disruption of this interaction both reduced TET2 phosphorylation and decreased TET2 stability. Furthermore, we noted that protein phosphatase 2A can interact with TET2 and dephosphorylate Ser-99. Collectively, these results provide detailed insights into the role of the TET2 N-terminal domain in TET2 regulation. Moreover, they reveal the dynamic nature of TET2 protein regulation that could have therapeutic implications for disease states resulting from reduced TET2 levels or activity.
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Registered trials
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