ミトーシスアクティベーター,p80cdc25の補充は,ヒトのタンパク質チロシンフォスファタゼによって行われます
Science (New York, N.Y.)
|December 14, 1990
まとめ
ミトスの侵入には,pp34タンパク質キナーゼの活性化が必要です. この研究では,Tyr15の脱リン酸化が pp34-サイクリン複合体の活性化を誘発し,ヒトのタンパク質チロシンフォスファタゼを巻き込み,それをcdc25経路とリンクすることを示しています.
科学分野:
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
- バイオケミストリー バイオケミストリー
背景:
- M相の発症は,eukaryotesのpp34タンパク質キナーゼ活性化に依存する.
- Schizosaccharomyces pombeでは,Tyr15によるpp34のリン酸化がミトーシスの開始を調節する.
- Tyr15の脱リン酸化は,細胞サイクル進行の重要な規制ステップです.
研究 の 目的:
- pp34活性化におけるTyr15脱酸化の役割を調査する.
- Tyr15の脱リン酸化に責任のあるフォスファターゼを特定する.
- ティロシン脱リン酸化とcdc25経路との関連を解明する.
主な方法:
- 分裂酵母とヒトのタンパク質チロシン・フォスファタゼを用いたインビトロおよびインビボ試験.
- pp34-サイクリン複合体の活性化の分析.
- 経路の置換を評価するための補完的なDNA (cDNA) 分析.
主要な成果:
- Tyr15の脱酸化は,分裂酵母におけるpp34-サイクリン複合体の活性化を直接引き起こす.
- ヒトのタンパク質チロシン・フォスファタゼは,この脱リン酸化現象を効果的に触媒化する.
- pp34の活性化には,スレオニン脱リン酸化は必要ありません.
- タイロシンフォスファタゼのcDNAは,p80cdc25を機能的に置き換え,経路関連性を示した.
結論:
- タイロシン脱リン酸化は,pp34-サイクリン複合体を活性化することによって,ミトーシスを開始するための重要なイベントです.
- ヒトのタンパク質チロシンファスファテーゼは,この調節機能を果たし,保存されたメカニズムを示唆します.
- この発見は,pp34のチロシン脱リン酸化と,cdc25媒介のミトシス活性化経路との間の直接的な関連性を確立しています.
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