Detection and Repair of Ionizing Radiation-Induced DNA Double Strand Breaks: New Developments in Nonhomologous End Joining

被引：115
|
作者：
Wang, Chen
Lees-Miller, Susan P.
机构：
[1] Univ Calgary, Dept Biochem & Mol Biol, Calgary, AB T2N 4N1, Canada
[2] Univ Calgary, Dept Oncol, Calgary, AB T2N 4N1, Canada
[3] Univ Calgary, Southern Alberta Canc Res Inst, Calgary, AB T2N 4N1, Canada
来源：
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS | 2013年 / 86卷 / 03期
基金：
美国国家卫生研究院; 加拿大健康研究院;
关键词：
DEPENDENT PROTEIN-KINASE; XRCC4-DNA LIGASE-IV; PHOSPHATIDYLINOSITOL 3-KINASE INHIBITOR; CATALYTIC SUBUNIT; DAMAGE RESPONSE; V(D)J RECOMBINATION; POLYNUCLEOTIDE KINASE/PHOSPHATASE; PHOSPHORYLATION SITES; KU HETERODIMER; PATHWAY CHOICE;
D O I：
10.1016/j.ijrobp.2013.01.011
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
DNA damage can occur as a result of endogenous metabolic reactions and replication stress or from exogenous sources such as radiation therapy and chemotherapy. DNA double strand breaks are the most cytotoxic form of DNA damage, and defects in their repair can result in genome instability, a hallmark of cancer. The major pathway for the repair of ionizing radiation-induced DSBs in human cells is nonhomologous end joining. Here we review recent advances on the mechanism of nonhomologous end joining, as well as new findings on its component proteins and regulation. (C) 2013 Elsevier Inc.
引用
收藏
页码：440 / 449
页数：10
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