The ATM protein kinase: regulating the cellular response to genotoxic stress, and more

被引：1236

作者：

Shiloh, Yosef ^{[1
]}

Ziv, Yael ^{[1
]}

机构：

[1] Tel Aviv Univ, Sackler Sch Med, David & Inez Myers Lab Canc Genet, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2013年 / 14卷 / 04期

基金：

以色列科学基金会;

关键词：

DOUBLE-STRAND BREAKS; DNA-DAMAGE RESPONSE; ATAXIA-TELANGIECTASIA GENE; NIGRO-STRIATAL NEURONS; NF-KAPPA-B; DEPENDENT PHOSPHORYLATION; IONIZING-RADIATION; HOMOLOGOUS RECOMBINATION; FUNCTIONAL-LINK; ACTIVATES ATM;

D O I：

10.1038/nrm3546

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signalling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. Although most ATM research has focused on this function, evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress. Moreover, it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.

引用

收藏

页码：197 / 210

页数：14

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