論文

査読有り
2012年1月

Phosphorylation of human INO80 is involved in DNA damage tolerance

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Dai Kato
  • ,
  • Mayumi Waki
  • ,
  • Masaki Umezawa
  • ,
  • Yuka Aoki
  • ,
  • Takahiko Utsugi
  • ,
  • Masaya Ohtsu
  • ,
  • Yasufumi Murakami

417
1
開始ページ
433
終了ページ
438
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2011.11.134
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Double strand breaks (DSBs) are the most serious type of DNA damage. DSBs can be generated directly by exposure to ionizing radiation or indirectly by replication fork collapse. The DNA damage tolerance pathway, which is conserved from bacteria to humans, prevents this collapse by overcoming replication blockages. The INO80 chromatin remodeling complex plays an important role in the DNA damage response. The yeast INO80 complex participates in the DNA damage tolerance pathway. The mechanisms regulating yINO80 complex are not fully understood, but yeast INO80 complex are necessary for efficient proliferating cell nuclear antigen (PCNA) ubiquitination and for recruitment of Rad18 to replication forks. In contrast, the function of the mammalian INO80 complex in DNA damage tolerance is less clear. Here, we show that human INO80 was necessary for PCNA ubiquitination and recruitment of Rad18 to DNA damage sites. Moreover, the C-terminal region of human INO80 was phosphorylated, and overexpression of a phosphorylation-deficient mutant of human INO80 resulted in decreased ubiquitination of PCNA during DNA replication. These results suggest that the human INO80 complex, like the yeast complex, was involved in the DNA damage tolerance pathway and that phosphorylation of human INO80 was involved in the DNA damage tolerance pathway. These findings provide new insights into the DNA damage tolerance pathway in mammalian cells. (C) 2011 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2011.11.134
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/22166198
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000299491600074&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2011.11.134
  • ISSN : 0006-291X
  • PubMed ID : 22166198
  • Web of Science ID : WOS:000299491600074

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