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Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells
http://hdl.handle.net/2297/29262
http://hdl.handle.net/2297/292621d4b7ff0-79c4-46c9-8fac-1955db1551bc
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
PH-PR-MATSUNAGA-T-1104.pdf (2.7 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-04 | |||||
| タイトル | ||||||
| タイトル | Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Matsumoto, Megumi
× Matsumoto, Megumi× Yaginuma, Kie× Igarashi, Ai× Imura, Mayumi× Hasegawa, Mizuho× Iwabuchi, Kuniyoshi× Date, Takayasu× Mori, Toshio× Ishizaki, Kanji× Yamashita, Katsumi× Inobe, Manabu× Matsunaga, Tsukasa |
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| 書誌情報 |
Journal of Cell Science 巻 120, 号 6, p. 1104-1112, 発行日 2007-03-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0021-9533 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00694823 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1242/jcs.03391 | |||||
| 出版者 | ||||||
| 出版者 | Company of Biologists | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Human histone H2AX is rapidly phosphorylated on serine 139 in response to DNA double-strand breaks and plays a crucial role in tethering the factors involved in DNA repair and damage signaling. Replication stress caused by hydroxyurea or UV also initiates H2AX phosphorylation in S-phase cells, although UV induced H2AX phosphorylation in non-cycling cells has recently been observed. Here we study the UV induced H2AX phosphorylation in human primary fibroblasts under growth-arrested conditions. This reaction absolutely depends on nucleotide excision repair (NER) and is mechanistically distinct from the replication stress-induced phosphorylation. The treatment of cytosine-β-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions. Consistently, the phosphorylation appears to be mainly mediated by ataxia-telangiectasia mutated and Rad3-related (ATR), although Chk1 (Ser345) is not phosphorylated by the activated ATR. The cellular levels of DNA polymerases δ and ε and proliferating cell nuclear antigen are markedly reduced in quiescent cells. We propose a model that perturbed gap-filling synthesis following dual incision in NER generates single-strand DNA gaps and hence initiates H2AX phosphorylation by ATR with the aid of RPA and ATRIP. | |||||
| 権利 | ||||||
| 権利情報 | Copyright © The Company of Biologists Limited 2007 | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://jcs.biologists.org/content/120/6/1104 | |||||
