Abstract
The Ten-eleven translocation (TET) family proteins are evolutionarily conserved dioxygenases responsible for the conversion of 5-methylcytosine to 5-hydroxymethylcytosine, thereby promoting DNA demethylation. There are three members in this family, namely TET1, TET2, and TET3. They contain structural features conferring unique substrate specificity and cofactor requirements and are subject to transcriptional control by transcription factors and microRNAs, and to posttranslational regulation by protein modifications and interacting proteins. TET2 is highly expressed in hematopoietic cells and plays a key role in hematopoiesis by controlling hematopoietic stem cell self-renewal, lineage commitment, and terminal differentiation. Analysis of TET2 knockout mice demonstrated a tumor suppressor function of TET2 whose loss and haplo-insufficiency initiate myeloid and lymphoid malignancies. TET2 inactivation, through loss-of-function mutations and isocitrate dehydrogenase 1 and 2 (IDH1/2) mutations, is a common event in hematopoietic malignancies. Understanding the structure, regulation, and function of TET2 should provide a better strategy to treat hematological malignancies.
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