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タイトル: | Functional role of NBS1 in radiation damage response and translesion DNA synthesis |
著者: | Saito, Yuichiro Komatsu, Kenshi |
著者名の別形: | 小松, 賢志 |
キーワード: | Chromatin remodeling DNA repair Homologous recombination NBS1 Translesion DNA synthesis |
発行日: | 20-Aug-2015 |
出版者: | MDPI AG |
誌名: | Biomolecules |
巻: | 5 |
号: | 3 |
開始ページ: | 1990 |
終了ページ: | 2002 |
抄録: | Nijmegen breakage syndrome (NBS) is a recessive genetic disorder characterized by increased sensitivity to ionizing radiation (IR) and a high frequency of malignancies. NBS1, a product of the mutated gene in NBS, contains several protein interaction domains in the N-terminus and C-terminus. The C-terminus of NBS1 is essential for interactions with MRE11, a homologous recombination repair nuclease, and ATM, a key player in signal transduction after the generation of DNA double-strand breaks (DSBs), which is induced by IR. Moreover, NBS1 regulates chromatin remodeling during DSB repair by histone H2B ubiquitination through binding to RNF20 at the C-terminus. Thus, NBS1 is considered as the first protein to be recruited to DSB sites, wherein it acts as a sensor or mediator of DSB damage responses. In addition to DSB response, we showed that NBS1 initiates Polη-dependent translesion DNA synthesis by recruiting RAD18 through its binding at the NBS1 C-terminus after UV exposure, and it also functions after the generation of interstrand crosslink DNA damage. Thus, NBS1 has multifunctional roles in response to DNA damage from a variety of genotoxic agents, including IR. |
著作権等: | © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
URI: | http://hdl.handle.net/2433/218415 |
DOI(出版社版): | 10.3390/biom5031990 |
PubMed ID: | 26308066 |
出現コレクション: | 学術雑誌掲載論文等 |
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