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プロアポプトティックBIDは,DNA損傷反応におけるATM効果因子である
Iris Kamer1, Rachel Sarig, Yehudit Zaltsman
1Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel.
Cell
|August 27, 2005
まとめ
BH3のみのタンパク質BIDは,DNA損傷後のアポトーシスと細胞サイクル停止に不可欠です. ATMキナーゼによるリン酸化は,これらのプロセスに不可欠であり,細胞死と生存における二重の役割を示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- バイオケミストリー バイオケミストリー
背景:
- BIDのようなBH3のみのタンパク質は,アポトーシスの重要な調節因子である.
- DNA損傷は,細胞サイクル停止とアポトーシスを含む細胞反応を誘発する.
研究 の 目的:
- DNA損傷によるアポトーシスと細胞周期調節におけるBIDタンパク質の役割を調査する.
- DNAの二重鎖の断裂後のBIDのリン酸化のメカニズムを解明する.
主な方法:
- BID.の細胞局所化研究.
- DNA損傷に対する反応としてBIDのリン酸化の分析.
- BIDのノックアウト細胞とBIDの変異体を細胞サイクル停止試験で使用する.
- トポイソメラーゼII毒であるエトポシドによる治療.
主要な成果:
- BIDは,健康な細胞の核に部分的に局所する.
- BIDは,DNAの二重鎖の断裂後の2つのコンセンサスサイトでATMキナーゼによってリン酸化される.
- BIDのノックアウト細胞は,エトポシド治療後のS相で停止することができません.
- 野生型BIDの回復はS相停止を救ったが,非リン酸化BID変異体はそうしなかった.
結論:
- BIDは,DNA損傷に対するATMキナーゼの効果因子である.
- BIDのリン酸化はS相停止に不可欠である.
- また,プロアポプトティックBIDは,DNA損傷反応において,プロサバイバル的な役割を果たす可能性があります.
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