NBS1 is required for ATRIP focus formation

DOI
  • KATO Akihiro
    Department of Genome Dynamics, Radiation Biology Center, Kyoto University
  • HATSUMURA Hiroteru
    Department of Genome Dynamics, Radiation Biology Center, Kyoto University
  • KOMATSU Kenshi
    Department of Genome Dynamics, Radiation Biology Center, Kyoto University

Bibliographic Information

Other Title
  • NBS1はATRIPのフォーカス形成に必要である

Description

The ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) protein kinases, which are members of phosphatidyl inositol 3-kinase-like kinase family, play central roles in DNA damage checkpoints. ATM is primarily activated by DNA double-strand breaks (DSBs) caused by ionizing radiation or radiomimetic drugs. Activation of ATM is stimulated by the MRE11-RAD50-NBS1 (MRN) complex. On the other hand, in response to UV damage or other replication blocking stress, ATR is activated by TopBP1 and phosphorylates several substrates, including Chk1. In the NBS1 deficient cells, Chk1 phosphorylation after UV irradiation is impaired, suggesting that activation of the ATR-mediated pathway also requires NBS1. However, its precise mechanism is unknown. In this study, we investigated whether NBS1 is required for ATR localization to DNA damage sites after UV irradiation. Roles of NBS1 in the ATR pathway will be discussed.

Journal

Keywords

Details 詳細情報について

  • CRID
    1390282680617836928
  • NII Article ID
    130007000667
  • DOI
    10.11513/jrrsabst.2008.0.123.0
  • Text Lang
    ja
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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