Role of non-homologous end joining (NHEJ) in maintaining genomic integrity
- 作者：Sandeep Burma ; Benjamin P.C. Chen and David J. Chen
- 关键词：Genomic instability ; Carcinogenesis ; Non-homologous end joining (NHEJ) ; DNA double-strand break (DSB) DNA-dependent protein kinase (DNA-PK)
- 刊名：DNA Repair
- 出版年：2006
- 期刊代码：121_15687864
- 类别：ch
- 出版时间：8 September 2006
- 卷：5
- 期：9-10
- 页码：1042-1048
- 文件大小：150 K
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 X-rays or γ-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.