ATM protein kinase: the linchpin of cellular defenses to stress

被引：92

作者：

Bhatti, Shahzad ^{[2
]}

Kozlov, Sergei ^{[1
]}

Farooqi, Ammad Ahmad ^{[2
]}

Naqi, Ali ^{[2
]}

Lavin, Martin ^{[1
]}

Khanna, Kum Kum ^{[1
]}

机构：

[1] Queensland Inst Med Res, QIMR, Brisbane, Qld 4029, Australia

[2] Univ Lahore, Inst Mol Biol & Biotechnol, Lahore, Pakistan

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2011年 / 68卷 / 18期

基金：

英国医学研究理事会; 澳大利亚研究理事会;

关键词：

ATM kinase; DNA damage response; Signaling; Carcinogenesis; DOUBLE-STRAND BREAKS; DNA-DAMAGE RESPONSE; TELANGIECTASIA MUTATED ATM; S-PHASE CHECKPOINT; ATAXIA-TELANGIECTASIA; IONIZING-RADIATION; OXIDATIVE STRESS; DEPENDENT PHOSPHORYLATION; MRE11/RAD50/NBS1; COMPLEX; INSULIN-RESISTANCE;

D O I：

10.1007/s00018-011-0683-9

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：

ATM is the most significant molecule involved in monitoring the genomic integrity of the cell. Any damage done to DNA relentlessly challenges the cellular machinery involved in recognition, processing and repair of these insults. ATM kinase is activated early to detect and signal lesions in DNA, arrest the cell cycle, establish DNA repair signaling and faithfully restore the damaged chromatin. ATM activation plays an important role as a barrier to tumorigenesis, metabolic syndrome and neurodegeneration. Therefore, studies of ATM-dependent DNA damage signaling pathways hold promise for treatment of a variety of debilitating diseases through the development of new therapeutics capable of modulating cellular responses to stress. In this review, we have tried to untangle the complex web of ATM signaling pathways with the purpose of pinpointing multiple roles of ATM underlying the complex phenotypes observed in AT patients.

引用

页码：2977 / 3006

页数：30

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