cdc25は,p34cdc2を直接活性化する特定のチロシンフォスファタゼです
J Gautier1, M J Solomon, R N Booher
1Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448.
Cell
|October 4, 1991
まとめ
CDC25タンパク質フォスファタゼは,チロシンに対するp34cdc2を特定的にデフォスフォリレートし,サイクリン-p34cdc2複合体を活性化し,Xenopus卵細胞のM相を開始します.
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:
- 細胞の循環は,タンパク質キナーゼとフォスファタゼによって調節されます.
- CDC25は細胞循環の重要な調節体であり,サイクリン-p34cdc2複合体の活動を制御する.
- CDC25のフォスファタゼ活性と基板特異性の正確なメカニズムは調査中です.
研究 の 目的:
- CDC25タンパク質の酵素活性と基板特異性を調査する.
- CDC25がp34cdc2を直接分解し,M相への入り口を調節するかどうかを判断する.
- p34cdc2.2.のリン酸化状態の制御におけるCDC25の役割を特徴づける.
主な方法:
- 細菌および酵母系におけるドロソフィラCDC25の発現.
- 細菌で発現したp34cdc2.2.を用いたインビトロフォスファターゼアッセイ.
- Xenopusの卵細胞と卵抽出物におけるM相誘導の分析.
- CDC25の推定的触媒部位のサイト指向型変異.
主要な成果:
- ドロソフィラCDC25は,不活性なサイクリン-p34cdc2を活性化し,Xenopus卵細胞のM相を誘導する.
- CDC25は,タンパク質チロシンフォスファタゼとシーケンスホモロジーを示しています.
- 細菌で発現するCDC25は,Tyr-15のp34cdc2をin vitroで特異的にデフォスフォリレートする.
- 触媒部位における突然変異は,インビトロおよびインビボの両方のCDC25活動を廃止する.
- CDC25は,p34cdc2に対して高い特異性を示し,他のチロシン・リン酸化タンパク質の脱リン酸化は最小限にしています.
結論:
- CDC25は,Tyr-15.5のp34cdc2を直接分解する特定のタンパク質チロシンファスファターゼです.
- この脱リン酸化イベントは,サイクリン-p34cdc2複合体の活性化とM相の開始に不可欠です.
- CDC25は,p34cdc2.2.の特定の脱リン化によって,MPF (成熟促進因子) の活性化を調節する上で重要な役割を果たしています.
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