TET2 in Normal and Malignant Hematopoiesis

被引：71

作者：

Bowman, Robert L. ^{[1
]}

Levine, Ross L. ^{[1
,2
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10021 USA

[2] Mem Sloan Kettering Canc Ctr, Dept Med, Leukemia Serv, New York, NY 10021 USA

来源：

COLD SPRING HARBOR PERSPECTIVES IN MEDICINE | 2017年 / 7卷 / 08期

关键词：

CELL SELF-RENEWAL; GENETIC-CHARACTERIZATION; DNA DEMETHYLATION; MUTATIONS RESULT; CXXC DOMAIN; STEM-CELLS; 5-METHYLCYTOSINE; EXPRESSION; PATHWAY; 5-HYDROXYMETHYLCYTOSINE;

D O I：

10.1101/cshperspect.a026518

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The ten-eleven translocation (TET) family of enzymes were originally cloned from the translocation breakpoint of t(10; 11) in infant acute myeloid leukemia (AML) with subsequent genomic analyses revealing somatic mutations and suppressed expression of TET family members across a range of malignancies, particularly enriched in hematological neoplasms. The TET family of enzymes is responsible for the hydroxylation of 5-methylcytosines (5-mC) to 5-hydroxymethylcytosine (5-hmC), followed by active and passive mechanisms leading to DNA demethylation. Given the complexity and importance of DNA methylation events in cellular proliferation and differentiation, it comes as no surprise that the TET family of enzymes is intricately regulated by both small molecules and regulatory cooperating proteins. Here, we review the structure and function of TET2, its interactions with cooperating mutations and small molecules, and its role in aberrant hematopoiesis.

引用

页数：11

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