T細胞におけるイオノミシンによるCD45タンパク質チロシンフォスファタゼ活性への負の調節
H L Ostergaard1, I S Trowbridge
1Department of Cancer Biology, Salk Institute, San Diego, CA 92186.
Science (New York, N.Y.)
|September 20, 1991
まとめ
イオノミシンによって誘発される細胞内カルシウムの増加は,T細胞におけるCD45タンパク質チロシンフォスファターゼ (PTPase) の活性を低下させます. これは,セリン脱リン酸化が,体内でのCD45 PTPase機能を調節する可能性があることを示唆しています.
科学分野:
- 免疫学 免疫学とは
- 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:
- CD45は,T細胞の反応に不可欠な白血球特異のタンパク質チロシンフォスファターゼ (PTPase) である.
- PTPaseの活性のインビヴォの調節は,依然としてほとんど特徴づけられていない.
研究 の 目的:
- CD45 PTPaseの活性のインビボ調節を調査する.
- CD45の活性を調節する細胞内カルシウムの役割を調査する.
主な方法:
- ネズミのチモサイトとT細胞系をカルシウムイオノフォールイオノミシンで治療する.
- CD45 PTPase活性に関する測定.
- CD45のリン酸化状態の分析,特にセリン残留の分析.
主要な成果:
- イオノミシン治療は,ネズミのチモサイトとT細胞系におけるCD45 PTPaseの活性を著しく低下させた.
- イオノミシン治療の後,CD45におけるセリン残基のリン酸化低下が観察されました.
結論:
- 細胞内カルシウムの増加は,体内においてCD45 PTPaseの活性を調節する.
- セリン脱リン酸化は,CD45 PTPase機能を調節する潜在的なメカニズムとして関与しています.
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