DNA demethylation by TDG

被引：8

作者：

Dalton, Shannon R. ^{[1
]}

Bellacosa, Alfonso ^{[1
]}

机构：

[1] Fox Chase Canc Ctr, Canc Biol Program, Epigenet & Progenitor Cells Program, Philadelphia, PA 19111 USA

来源：

EPIGENOMICS | 2012年 / 4卷 / 04期

关键词：

5-carboxylcytosine; 5-formylcytosine; 5-hydroxymethylcytosine; 5-hydroxymethyluracil; base excision repair; DNA demethylation; DNA methylation; embryonic lethality; histone modification; thymine DNA glycosylase; MOUSE FETAL-DEVELOPMENT; ACUTE MYELOID-LEUKEMIA; BASE-EXCISION-REPAIR; THYMINE-DNA; EMBRYONIC LETHALITY; ACTIVE-DEMETHYLATION; 5-METHYLCYTOSINE-DNA GLYCOSYLASE; MAMMALIAN DEVELOPMENT; TARGETED DISRUPTION; CANCER EPIGENETICS;

D O I：

10.2217/EPI.12.36

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

DNA methylation has long been considered a very stable DNA modification in mammals that could only be removed by replication in the absence of remethylation - that is, by mere dilution of this epigenetic mark (so-called passive DNA demethylation). However, in recent years, a significant number of studies have revealed the existence of active processes of DNA demethylation in mammals, with important roles in development and transcriptional regulation, allowing the molecular mechanisms of active DNA demethylation to be unraveled. In this article, we review the recent literature highlighting the prominent role played in active DNA demethylation by base excision repair and especially by TDG.

引用

页码：459 / 467

页数：9

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