The role of ATM and ATR in DNA damage-induced cell cycle control.

Progress in cell cycle research Pub Date : 2003-01-01
Aaron A Goodarzi, Wesley D Block, Susan P Lees-Miller
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引用次数: 0

Abstract

Ataxia-Telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) are members of the phosphatidyl inositol 3-kinase-like family of serine/threonine protein kinases (PIKKs), and play important roles in the cellular response to DNA damage. Activation of ATM by ionizing radiation results in the activation of signal transduction pathways that induce cell cycle arrest at G1/S, S and G2/M. ATR is required for cell cycle arrest in response to DNA-damaging agents such as ultraviolet radiation that cause bulky lesions. This review focuses on the role of ATM and ATR in various DNA damage response pathways, and discusses the potential for targeting these pathways for the development of novel therapeutics.

ATM和ATR在DNA损伤诱导的细胞周期控制中的作用。
ataxia - telangiexpansion mutated (ATM)和ATM- and Rad3-related (ATR)是磷脂酰肌醇3-激酶样丝氨酸/苏氨酸蛋白激酶(PIKKs)家族的成员,在细胞对DNA损伤的反应中起重要作用。电离辐射激活ATM导致信号转导通路的激活,诱导细胞周期阻滞在G1/S、S和G2/M。ATR是细胞周期阻滞所必需的,以响应dna损伤剂,如引起大面积病变的紫外线辐射。本文综述了ATM和ATR在多种DNA损伤反应途径中的作用,并讨论了针对这些途径开发新疗法的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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