DNA End Resection:Facts and Mechanisms

被引：0

作者：

Ting Liu ^{[1
]}

Jun Huang ^{[2
]}

机构：

[1] Department of Cell Biology and Program in Molecular Cell Biology,Zhejiang University School of Medicine

[2] Life Sciences Institute and Innovation Center for Cell Signaling Network,Zhejiang University

来源：

Genomics,Proteomics & Bioinformatics | 2016年 / 14卷 / 03期

基金：

中国国家自然科学基金; 高等学校博士学科点专项科研基金; 中央高校基本科研业务费专项资金资助;

关键词：

DNA end resection; Homologous recombination; DNA double-strand breaks; Chromatin remodeling factors; Genome stability;

D O I：

暂无

中图分类号：

Q78 [基因工程（遗传工程）];

学科分类号：

071007 ; 0836 ; 090102 ;

摘要：

DNA double-strand breaks(DSBs),which arise following exposure to a number of endogenous and exogenous agents,can be repaired by either the homologous recombination(HR)or non-homologous end-joining(NHEJ) pathways in eukaryotic cells.A vital step in HR repair is DNA end resection,which generates a long 30single-stranded DNA(ss DNA) tail that can invade the homologous DNA strand.The generation of 30 ss DNA is not only essential for HR repair,but also promotes activation of the ataxia telangiectasia and Rad3-related protein(ATR).Multiple factors,including the MRN/X complex,C-terminal-binding protein interacting protein(Ct IP)/Sae2,exonuclease 1(EXO1),Bloom syndrome protein(BLM)/Sgs1,DNA2 nuclease/helicase,and several chromatin remodelers,cooperate to complete the process of end resection.Here we review the basic machinery involved in DNA end resection in eukaryotic cells.

引用

页码：126 / 130

页数：5

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