生物
免疫系统
表观遗传学
DNA去甲基化
癌症
免疫疗法
5-羟甲基胞嘧啶
免疫学
DNA
癌变
去甲基化
癌症研究
DNA甲基化
遗传学
基因
基因表达
作者
Isaac F. López-Moyado,Myunggon Ko,Patrick G. Hogan,Anjana Rao
出处
期刊:Annual Review of Immunology
[Annual Reviews]
日期:2024-02-16
卷期号:42 (1): 455-488
被引量:8
标识
DOI:10.1146/annurev-immunol-080223-044610
摘要
Ten-eleven translocation (TET) proteins are iron-dependent and α-ketoglutarate-dependent dioxygenases that sequentially oxidize the methyl group of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). All three epigenetic modifications are intermediates in DNA demethylation. TET proteins are recruited by transcription factors and by RNA polymerase II to modify 5mC at enhancers and gene bodies, thereby regulating gene expression during development, cell lineage specification, and cell activation. It is not yet clear, however, how the established biochemical activities of TET enzymes in oxidizing 5mC and mediating DNA demethylation relate to the known association of TET deficiency with inflammation, clonal hematopoiesis, and cancer. There are hints that the ability of TET deficiency to promote cell proliferation in a signal-dependent manner may be harnessed for cancer immunotherapy. In this review, we draw upon recent findings in cells of the immune system to illustrate established as well as emerging ideas of how TET proteins influence cellular function.
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