ATR: a master conductor of cellular responses to DNA replication stress

被引：231

作者：

Flynn, Rachel Litman ^{[1
]}

Zou, Lee ^{[1
,2
]}

机构：

[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Charlestown, MA 02129 USA

[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2011年 / 36卷 / 03期

基金：

美国国家卫生研究院;

关键词：

INTERSTRAND CROSS-LINK; S-PHASE CHECKPOINT; FANCONI-ANEMIA PATHWAY; CHROMATIN REMODELING COMPLEX; HOLLIDAY JUNCTION RESOLVASE; DAMAGE CHECKPOINT; STRANDED-DNA; MONOUBIQUITINATED FANCD2; SIGNALING PATHWAYS; POLYMERASE-ALPHA;

D O I：

10.1016/j.tibs.2010.09.005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The integrity of the genome is constantly challenged by intrinsic and extrinsic genotoxic stresses that damage DNA. The cellular responses to DNA damage are orchestrated by DNA damage signaling pathways, also known as DNA damage checkpoints. These signaling pathways play crucial roles in detecting DNA damage, regulating DNA repair and coordinating DNA repair with other cellular processes. In vertebrates, the ATM- and Rad3-related (ATR) kinase plays a key role in the response to a broad spectrum of DNA damage and DNA replication stress. Here, we will discuss the recent findings on how ATR is activated by DNA damage and how it protects the genome against interference with DNA replication.

引用

页码：133 / 140

页数：8

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