DNA-PK: A dynamic enzyme in a versatile DSB repair pathway

被引：260

作者：

Davis, Anthony J. ^{[1
]}

Chen, Benjamin P. C. ^{[1
]}

Chen, David J. ^{[1
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Div Mol Radiat Biol, Dept Radiat Oncol, Dallas, TX 75390 USA

来源：

DNA REPAIR | 2014年 / 17卷

基金：

美国国家卫生研究院;

关键词：

DNA double strand breaks; Non-homologous end-joining; Ku70/80; DNA-PKcs; XRCC4; DNA ligase IV; XLF; DEPENDENT PROTEIN-KINASE; DOUBLE-STRAND-BREAK; XRCC4-DNA LIGASE-IV; END-JOINING PATHWAY; HUMAN TUMOR-CELLS; CATALYTIC SUBUNIT; IONIZING-RADIATION; PHOSPHORYLATION SITES; V(D)J RECOMBINATION; HOMOLOGOUS RECOMBINATION;

D O I：

10.1016/j.dnarep.2014.02.020

中图分类号：

Q3 [遗传学];

学科分类号：

071007 [遗传学];

摘要：

DNA double stranded breaks (DSBs) are the most cytoxic DNA lesion as the inability to properly repair them can lead to genomic instability and tumorigenesis. The prominent DSB repair pathway in humans is non-homologous end-joining (NHEJ). In the simplest sense, NHEJ mediates the direct re-ligation of the broken DNA molecule. However, NHEJ is a complex and versatile process that can repair DSBs with a variety of damages and ends via the utilization of a significant number of proteins. In this review we will describe the important factors and mechanisms modulating NHEJ with emphasis given to the versatility of this repair process and the DNA-PR complex. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：21 / 29

页数：9

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