論文

査読有り
2007年12月

DDB1 gene disruption causes a severe growth defect and apoptosis in chicken DT40 cells

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Mitsuo Wakasugi
  • ,
  • Kenkyo Matsuura
  • ,
  • Atsushi Nagasawa
  • ,
  • DongTao Fu
  • ,
  • Hiroko Shimizu
  • ,
  • Ken-ichi Yamamoto
  • ,
  • Shunichi Takeda
  • ,
  • Tsukasa Matsunaga

364
4
開始ページ
771
終了ページ
777
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2007.10.063
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

DDB1 was originally identified as a heterodimeric complex with DDB2 and plays an accessory role in nucleotide excision repair. DDB1 also constitutes an E3 ubiquitin ligase complex together with Cul4A and Roc1 and acts as an adaptor, suggesting its multiple roles beyond DNA repair. We have generated a conditional DDB1-knockout mutant using a chicken B lymphocyte line DT40. Doxycycline-induced DDB1 depletion caused a severe growth defect followed by apoptotic cell death. Flow cytometric analyses revealed that cell cycle progression is initially retarded at all phases and subsequently impaired at S phase along with the appearance of sub-G1 population. Similarly, DDB1-knockdown in human U2OS cells by small interfering RNA exhibited a loss of clonogenic activity and perturbed cell cycle progression. These results demonstrate that the DDB1 gene is indispensable for cell viability in higher vertebrates and this conditional DDB1-knockout clone would be highly useful for the functional analysis of DDB1. (C) 2007 Elsevier Inc. All rights reserved.

Web of Science ® 被引用回数 : 12

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2007.10.063
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/17976535
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000251358500010&DestApp=WOS_CPL
URL
http://europepmc.org/abstract/med/17976535
URL
http://orcid.org/0000-0003-4612-6031
ID情報
  • DOI : 10.1016/j.bbrc.2007.10.063
  • ISSN : 0006-291X
  • ORCIDのPut Code : 45674071
  • PubMed ID : 17976535
  • Web of Science ID : WOS:000251358500010

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