Regulation of CpG methylation by Dnmt and Tet in pluripotent stem cells

被引：21

作者：

Horii, Takuro ^{[1
]}

Hatada, Izuho ^{[1
]}

机构：

[1] Gunma Univ, Inst Mol & Cellular Regulat, Biosignal Genome Resource Ctr, Lab Genome Sci, Gunma 3718512, Japan

来源：

JOURNAL OF REPRODUCTION AND DEVELOPMENT | 2016年 / 62卷 / 04期

基金：

日本学术振兴会;

关键词：

CpG methylation; CRISPR/Cas; DNA methyltransferase; Embryonic stem cells; Ten-eleven translocation; DNA METHYLTRANSFERASE GENE; DE-NOVO METHYLATION; MAMMALIAN DNA; ES CELLS; IMMUNODEFICIENCY SYNDROME; MOUSE EMBRYOS; CANCER-CELLS; IN-VITRO; GENOME; DEMETHYLATION;

D O I：

10.1262/jrd.2016-046

中图分类号：

S8 [畜牧、动物医学、狩猎、蚕、蜂];

学科分类号：

0905 ;

摘要：

Vertebrate genomes are highly methylated at cytosine residues in CpG sequences. CpG methylation plays an important role in epigenetic gene silencing and genome stability. Compared with other epigenetic modifications, CpG methylation is thought to be relatively stable; however, it is sometimes affected by environmental changes, leading to epigenetic instability and disease. CpG methylation is reversible and regulated by DNA methyltransferases and demethylases including ten-eleven translocation. Here, we discuss CpG methylation instability and the regulation of CpG methylation by DNA methyltransferases and ten-eleven translocation in pluripotent stem cells.

引用

页码：331 / 335

页数：5

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