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タイトル: NBS1 and multiple regulations of DNA damage response
著者: Komatsu, Kenshi
著者名の別形: 小松, 賢志
キーワード: Nijmegen breakage syndrome
NBS1
RNF20
MRE11
ATM
RPA
RAD18
発行日: 16-Aug-2016
出版者: Oxford University Press
誌名: Journal of Radiation Research
巻: 57
号: S1
開始ページ: i11
終了ページ: i17
抄録: 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.
著作権等: © 2016 The Author 2016. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Radiation Oncology.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/ ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
URI: http://hdl.handle.net/2433/219573
DOI(出版社版): 10.1093/jrr/rrw031
出現コレクション:学術雑誌掲載論文等

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