Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation.
By Hao Wu, Yi Zhang. Genes & Development, 2011
675 citations recorded by the source corpus.
Ten-eleven translocation 1-3 (Tet1-3) proteins have recently been discovered in mammalian cells to be members of a family of DNA hydroxylases that possess enzymatic activity toward the methyl mark on the 5-position of cytosine (5-methylcytosine [5mC]), a well-characterized epigenetic modification that has essential roles in regulating gene expression and maintaining cellular identity. Tet proteins can convert 5mC into 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) through three consecutive oxidation reactions. These modified bases may represent new epigenetic states in genomic DNA or intermediates in the process of DNA demethylation. Emerging biochemical, genetic, and functional evidence suggests that Tet proteins are crucial for diverse biological processes, including zygotic epigenetic reprogramming, pluripotent stem cell differentiation, hematopoiesis, and development of leukemia. Insights into how Tet proteins contribute to dynamic changes in DNA methylation and gene expression will greatly enhance our understanding of epigenetic regulation of normal development and human diseases.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d02a5853ecad89ccef9d3c60f3d9a994fa8e8fc3
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Citations in the corpus
- Cancer epigenetics: from mechanism to therapy. (2012, background): “Consistent with the notion that 5hmC is likely to have a role in both transcriptional activation and silencing, the TET proteins have also been shown to have activating and repressive functions (Wu and Zhang, 2011).”
- TETonic shift: biological roles of TET proteins in DNA demethylation and transcription (2013, neutral): “TET proteins are named after the ten-eleven translocation (t(10;11)(q22;q23)) that is found in rare cases of acute myeloid and lymphocytic leukaemia.”
- A double take on bivalent promoters. (2013, background): “The presence of the TET enzymes at CpG islands may further ensure the GENES & DEVELOPMENT 1329 absence of DNA methylation at those sites (Wu and Zhang 2011; Williams et al. 2012).”
- Reversing DNA Methylation: Mechanisms, Genomics, and Biological Functions (2014, neutral): “Growing evidence suggests that impairment in TET-mediated DNA demethylation may contribute to tumorigenesis (Cimmino et al., 2011; Wu and Zhang, 2011a).”
- DNA base damage by reactive oxygen species, oxidizing agents, and UV radiation. (2013, background): “More recently, 5-carboxycytosine (5-CaCyt) was characterized as the ultimate enzymatic oxidation product of 5methylcytosine (Ito et al. 2011; Pfaffeneder et al. 2011; Wu and Zhang 2011; Zhang et al. 2012).”
- Epigenetic Determinants of Cancer. (2016, background): “Simultaneously, the TET1, -2, and -3 proteins (ten-eleven translocations) were shown to catalyze these oxidative steps (Wu and Zhang 2011a,b), suggesting that these are some of the effectors of active and/or passive DNA demethylation pathways (see Fig.”
- LOSS OF 5-HYDROXYMETHYLCYTOSINE IS AN EPIGENETIC HALLMARK OF MELANOMA (2012, background): “Thus, understanding the intricate relationship between the regulation of 5-hmC and associated gene transcription remains a challenge in 5-hmC biology (Cimmino et al., 2011; Wu and Zhang, 2011).”
- Analysing and interpreting DNA methylation data (2012, background): “What is the functional rel‑ evance of the recently discovered variants of DNA meth‑ ylation, including 5‑hydroxymethylcytosine (5hmC), 5‑formylcytosine and 5‑carboxylcytosine 141 ?”