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Other Stress Responses in Bacteria01:30

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幹細胞 の 機能 と ストレス 反応 は,タンパク質 の 合成 に よっ て 制御 さ れる

Sandra Blanco1, Roberto Bandiera1, Martyna Popis1

  • 1Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.

Nature
|June 17, 2016
PubMed
まとめ

細胞のストレス反応経路は,マウス皮膚幹細胞のタンパク質合成を減らし,幹細胞の機能と腫瘍の成長を促します. この抑制は組織や腫瘍の再生のために逆転する必要があります.

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科学分野:

  • 幹細胞生物学
  • 分子生物学
  • 癌の研究

背景:

  • 幹細胞の調節におけるタンパク質合成と細胞のストレス反応の相互作用は十分に理解されていません.
  • 幹細胞は 組織ホメオスタシスを維持し 損傷した組織を再生できる ユニークな性質を持っています

研究 の 目的:

  • ネズミの皮膚幹細胞機能を制御するタンパク質合成と細胞のストレス反応経路の相互作用を調査する.
  • 幹細胞による腫瘍形成と組織再生の基礎となる分子メカニズムを解明する.

主な方法:

  • 幹細胞とプロジェニタルのタンパク質合成を比較した in vivo 研究.
  • ストレス反応経路とトランスレーションプログラムの分析
  • 転写後のサイトシン-5メチル化の役割を調査する.

主要な成果:

  • ネズミの皮膚幹細胞は,増殖期においても,原始細胞と比較してタンパク質合成が減少している.
  • ストレス反応経路の活性化により,タンパク質合成が全般的に減少し,トランスレーションプログラムが変化し,幹細胞機能と腫瘍発生が促進されます.
  • 転写後のサイトシン5メチル化の阻害は,腫瘍を誘発する細胞におけるこの翻訳的阻害を維持し,矛盾的に細胞毒性ストレスに対する感受性を高め,腫瘍の再生を阻害する.

結論:

  • ストレス反応経路に起因する タンパク質合成の減少と変異したトランスレーションプログラムは 幹細胞機能と腫瘍発生に不可欠です
  • 細胞毒性ストレス後の組織と腫瘍の再生には,翻訳阻害の逆転が不可欠です.