ダウンロード数: 154
このアイテムのファイル:
ファイル | 記述 | サイズ | フォーマット | |
---|---|---|---|---|
eLife.32222.pdf | 1.28 MB | Adobe PDF | 見る/開く |
タイトル: | Distinct roles of ATM and ATR in the regulation of ARP8 phosphorylation to prevent chromosome translocations. |
著者: | Sun, Jiying Shi, Lin Kinomura, Aiko Fukuto, Atsuhiko Horikoshi, Yasunori Oma, Yukako Harata, Masahiko Ikura, Masae https://orcid.org/0000-0002-0426-8923 (unconfirmed) Ikura, Tsuyoshi Kanaar, Roland Tashiro, Satoshi |
著者名の別形: | 井倉, 正枝 井倉, 毅 |
発行日: | 8-May-2018 |
出版者: | eLife Sciences Publications, Ltd |
誌名: | eLife |
巻: | 7 |
論文番号: | e32222 |
抄録: | Chromosomal translocations are hallmarks of various types of cancers and leukemias. However, the molecular mechanisms of chromosome translocations remain largely unknown. The ataxia-telangiectasia mutated (ATM) protein, a DNA damage signaling regulator, facilitates DNA repair to prevent chromosome abnormalities. Previously, we showed that ATM deficiency led to the 11q23 chromosome translocation, the most frequent chromosome abnormalities in secondary leukemia. Here, we show that ARP8, a subunit of the INO80 chromatin remodeling complex, is phosphorylated after etoposide treatment. The etoposide-induced phosphorylation of ARP8 is regulated by ATM and ATR, and attenuates its interaction with INO80. The ATM-regulated phosphorylation of ARP8 reduces the excessive loading of INO80 and RAD51 onto the breakpoint cluster region. These findings suggest that the phosphorylation of ARP8, regulated by ATM, plays an important role in maintaining the fidelity of DNA repair to prevent the etoposide-induced 11q23 abnormalities. |
著作権等: | © 2018, Sun et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited. |
URI: | http://hdl.handle.net/2433/235195 |
DOI(出版社版): | 10.7554/eLife.32222 |
PubMed ID: | 29759113 |
出現コレクション: | 学術雑誌掲載論文等 |
このリポジトリに保管されているアイテムはすべて著作権により保護されています。