TET2 (ten-eleven translocation 2) encodes a Fe(II)/α-ketoglutarate-dependent dioxygenase that catalyzes the oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), thereby contributing to active DNA demethylation and epigenetic regulation of gene expression
[1][2]. TET2-mediated DNA demethylation is particularly important at promoters and enhancers, where it helps maintain chromatin accessibility and supports lineage-specific transcriptional programs during cellular differentiation
[3][4]. Mechanistically, TET2 regulates hematopoietic development by controlling enhancer methylation status and expression of genes required for hematopoietic stem and progenitor cell function
[4][3]. Consistent with this role, loss of TET2 disrupts normal hematopoiesis, promotes expansion of hematopoietic stem and progenitor compartments, and is strongly associated with myeloid malignancies including acute myeloid leukemia and related hematologic disorders
[1][5][6]. Beyond hematopoiesis, TET2 also contributes to immune-cell regulation through epigenetic control of innate and adaptive immune responses
[5][7]. Compared with the related dioxygenases TET1 and TET3, TET2 shows a particularly prominent role in hematopoietic and immune-cell biology, whereas TET1 and TET3 preferentially occupy promoter-associated regions in several developmental contexts
[7]. For experimental applications, TET2 serves as a widely used model for studying DNA methylation dynamics, enhancer regulation, clonal hematopoiesis, leukemia pathogenesis, and epigenetic mechanisms underlying immune-cell differentiation and function
[4][5][6].