Functional role of ATM in the cellular response to DNA damage
Functional role of ATM in the cellular response to DNA damage
Ming LIU1, Wenxiang HU2()
1. College of Life Science, Capital Normal University, Beijing 100048, China; 2. Institute of Physical Organic and Medicinal Chemistry, Capital Normal University, Beijing 100048, China
Ataxia-telangiectasia mutated (ATM) plays a key role in regulating the cellular response to ionizing radiation. The tumor-suppressor gene ATM, mutations in which cause the human genetic disease ataxia telangiectasia, encodes a key protein kinase that controls the cellular response to double-stranded breaks. Activation of ATM results in phosphorylation of many downstream targets that modulate numerous damage response pathways, most notably cell cycle checkpoints. Here, we highlight some of the new developments in the field in our understanding of the mechanism of activation of ATM and its signaling pathways, explore whether DNA double-strand breaks are the sole activators of ATM and ATM-dependent signaling pathways, and address some of the prominent, unanswered questions related to ATM and its function. The scope of this article is to provide a brief overview of the recent literature on this subject and to raise questions that could be addressed in future studies.
Corresponding Author(s):
HU Wenxiang,Email:huwx66@163.com
引用本文:
. Functional role of ATM in the cellular response to DNA damage[J]. Frontiers of Chemical Science and Engineering, 2011, 5(2): 179-187.
Ming LIU, Wenxiang HU. Functional role of ATM in the cellular response to DNA damage. Front Chem Sci Eng, 2011, 5(2): 179-187.
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