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タイトル: | NBS1 is regulated by two kind of mechanisms: ATM-dependent complex formation with MRE11 and RAD50, and cell cycle–dependent degradation of protein |
著者: | Zhou, Hui Kawamura, Kasumi Yanagihara, Hiromi Kobayashi, Junya Zhang-Akiyama, Qiu-Mei |
著者名の別形: | 小林, 純也 秋山, 秋梅 |
キーワード: | DNA damage NBS1 ATM cell cycle checkpoint homologous recombination |
発行日: | Jul-2017 |
出版者: | Oxford University Press (OUP) |
誌名: | Journal of Radiation Research |
巻: | 58 |
号: | 4 |
開始ページ: | 487 |
終了ページ: | 494 |
抄録: | Nijmegen breakage syndrome (NBS), a condition similar to Ataxia-Telangiectasia (A-T), is a radiation-hypersensitive genetic disorder showing chromosomal instability, radio-resistant DNA synthesis, immunodeficiency, and predisposition to malignances. The product of the responsible gene, NBS1, forms a complex with MRE11 and RAD50 (MRN complex). The MRN complex is necessary for the DNA damage–induced activation of ATM. However, the regulation of MRN complex formation is still unclear. Here, we investigated the regulatory mechanisms of MRN complex formation. We used an immunoprecipitation assay to determine whether levels of the MRN complex were increased by radiation-induced DNA damage and found that the levels of these proteins and their mRNAs did not increase. ATM-dependent phosphorylation of NBS1 contributed to the DNA damage–induced MRN complex formation. However, pre-treatment of cells with an ATM-specific inhibitor did not affect homologous recombination (HR) and non-homologous end-joining (NHEJ) repair. G0 phase cells, decreasing NBS1 and HR activity but not NHEJ, gained HR-related chromatin association of RAD51 by overexpression of NBS1, suggesting that the amount of NBS1 may be important for repressing accidental activation of HR. These evidences suggest that NBS1 is regulated by two kind of mechanisms: complex formation dependent on ATM, and protein degradation mediated by an unknown MG132-resistant pathway. Such regulation of NBS1 may contribute to cellular responses to double-strand breaks. |
記述: | A correction has been published: Journal of Radiation Research, Volume 59, Issue 2, March 2018, Page 243, |
著作権等: | © The Author 2017. 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. For commercial re-use, please contact journals.permissions@oup.com |
URI: | http://hdl.handle.net/2433/242248 |
DOI(出版社版): | 10.1093/jrr/rrx014 |
PubMed ID: | 28369484 |
関連リンク: | https://doi.org/10.1093/jrr/rrx069 |
出現コレクション: | 学術雑誌掲載論文等 |
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