Role of non-homologous end joining (NHEJ) in maintaining genomic integrity

被引：313

作者：

Burma, Sandeep ^{[1
]}

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

Chen, David J. ^{[1
]}

机构：

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

来源：

DNA REPAIR | 2006年 / 5卷 / 9-10期

关键词：

genomic instability; carcinogenesis; non-homologous end joining (NHEJ); DNA double-strand break (DSB); DNA-dependent protein kinase (DNA-PK);

D O I：

10.1016/j.dnarep.2006.05.026

中图分类号：

Q3 [遗传学];

学科分类号：

071007 [遗传学]; 090102 [作物遗传育种];

摘要：

Of the various types of DNA damage that can occur within the mammalian cell, the DNA double strand break (DSB) is perhaps the most dangerous. DSBs are typically induced by intrinsic sources such as the by products of cellular metabolism or by extrinsic sources such as Xrays or gamma-rays and chemotherapeutic drugs. It is becoming increasing clear that an inability to respond properly to DSBs will lead to genomic instability and promote carcinogenesis. The mammalian cell, therefore, has in place several mechanisms that can respond rapidly to DSBs. In this review, we focus on the role of one such mechanism, the non-homologous end joining (NHEJ) pathway of DSB repair, in maintaining genome integrity and preventing carcinogenesis. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：1042 / 1048

页数：7

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