ArticleNucleic acids research2016
A primary role of TET proteins in establishment and maintenance of De Novo bivalency at CpG islands.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Loss of ten-eleven translocation 2 (TET2) facilitates aggressive behaviour in cutaneous melanoma by inducing peroxisome proliferator-activated receptor-γ coactivator 1α expression and oxidative phosphorylation.The British journal of dermatology · 2026Article
- ACTC1 promotes tumor progression by upregulating BMP4 expression in prostate cancer.BMC cancer · 2025Article
- TET1: The epigenetic architect of clinical disease progression.Genes & diseases · 2025Review
- Cell identity and 5-hydroxymethylcytosine.Epigenetics & chromatin · 2025Review
- YEATS2: a novel cancer epigenetic reader and potential therapeutic target.Cancer cell international · 2025Review
- Identification of the specific characteristics of neuroendocrine prostate cancer: Immune status, hub genes and treatment.Translational oncology · 2025Article
- Metabolic regulation of the glioblastoma stem cell epitranscriptome by malate dehydrogenase 2.Cell metabolism · 2024Article
- Injured inflammatory environment overrides the TET2 shaped epigenetic landscape of pluripotent stem cell derived human neural stem cells.Scientific reports · 2024Article
- MYH6 suppresses tumor progression by downregulating KIT expression in human prostate cancer.Scientific reports · 2024Article
- Histone serotonylation in dorsal raphe nucleus contributes to stress- and antidepressant-mediated gene expression and behavior.Nature communications · 2024Article
- Dnmt1/Tet2-mediated changes in Cmip methylation regulate the development of nonalcoholic fatty liver disease by controlling the Gbp2-Pparγ-CD36 axis.Experimental & molecular medicine · 2023Article
- Tumour suppressor TET2 safeguards enhancers from aberrant DNA methylation and epigenetic reprogramming in ERα-positive breast cancer cells.Epigenetics · 2022Article
- Downregulation of PGM5 expression correlates with tumor progression and poor prognosis in human prostate cancer.Discover oncology · 2022Article
- TET2-mediated epigenetic reprogramming of breast cancer cells impairs lysosome biogenesis.Life science alliance · 2022Article
- The chromatin remodelling protein LSH/HELLS regulates the amount and distribution of DNA hydroxymethylation in the genome.Epigenetics · 2022Article
- DNA Hydroxymethylation in Smoking-Associated Cancers.International journal of molecular sciences · 2022Review
- ERα promotes transcription of tumor suppressor geneJournal of Zhejiang University. Science. B · 2021Article
- ZBTB38 suppresses prostate cancer cell proliferation and migration via directly promoting DKK1 expression.Cell death & disease · 2021Article
- Cyclic DNA remethylation following active demethylation at euchromatic regions in mouse embryonic stem cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2021Article
- TET2 InhibitsCancers · 2021Article
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Authors and funding
15 authors.
Funding
Abstract
Ten Eleven Translocation (TET) protein-catalyzed 5mC oxidation not only creates novel DNA modifications, such as 5hmC, but also initiates active or passive DNA demethylation. TETs' role in the crosstalk with specific histone modifications, however, is largely elusive. Here, we show that TET2-mediated DNA demethylation plays a primary role in the de novo establishment and maintenance of H3K4me3/H3K27me3 bivalent domains underlying methylated DNA CpG islands (CGIs). Overexpression of wild type (WT), but not catalytic inactive mutant (Mut), TET2 in low-TET-expressing cells results in an increase in the level of 5hmC with accompanying DNA demethylation at a subset of CGIs. Most importantly, this alteration is sufficient in making de novo bivalent domains at these loci. Genome-wide analysis reveals that these de novo synthesized bivalent domains are largely associated with a subset of essential developmental gene promoters, which are located within CGIs and are previously silenced due to DNA methylation. On the other hand, deletion of Tet1 and Tet2 in mouse embryonic stem (ES) cells results in an apparent loss of H3K27me3 at bivalent domains, which are associated with a particular set of key developmental gene promoters. Collectively, this study demonstrates the critical role of TET proteins in regulating the crosstalk between two key epigenetic mechanisms, DNA methylation and histone methylation (H3K4me3 and H3K27me3), particularly at CGIs associated with developmental genes.
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