文章基本信息
- 标题：NBS1 and multiple regulations of DNA damage response
- 本地全文：下载
- 作者：Kenshi Komatsu
- 期刊名称：Journal of Radiation Research
- 印刷版ISSN：0449-3060
- 电子版ISSN：1349-9157
- 出版年度：2016
- 卷号：57
- 期号：S1
- 页码：11-17
- DOI：10.1093/jrr/rrw031
- 摘要：DNA damage response is finely tuned, with several pathways including those for DNA repair, chromatin remodeling and cell cycle checkpoint, although most studies to date have focused on single pathways. Genetic diseases characterized by genome instability have provided novel insights into the underlying mechanisms of DNA damage response. NBS1, a protein responsible for the radiation-sensitive autosomal recessive disorder Nijmegen breakage syndrome, is one of the first factors to accumulate at sites of DNA double-strand breaks (DSBs). NBS1 binds to at least five key proteins, including ATM, RPA, MRE11, RAD18 and RNF20, in the conserved regions within a limited span of the C terminus, functioning in the regulation of chromatin remodeling, cell cycle checkpoint and DNA repair in response to DSBs. In this article, we reviewed the functions of these binding proteins and their comprehensive association with NBS1. © The Author 2016. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology.
- 关键词：ATM;MRE11;NBS1;Nijmegen breakage syndrome;RAD18;RNF20;RPA
