SRCは,ワクチンウイルスの微小管からアクチンベースの運動性への切り替えを媒介する
Timothy P Newsome1, Niki Scaplehorn, Michael Way
1Cell Motility Laboratory, Room 529, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.
Science (New York, N.Y.)
|August 7, 2004
まとめ
ワクチンウイルスのアクチンポリメリゼーションには,Src依存のA36Rリン酸化が必要です. ウイルスタンパク質B5RはSrcを活性化させ,A36Rのリン酸化を誘発し,細胞運動のためにキネシン募集を調節します.
科学分野:
- ウイルス学 ウイルス学 ウイルス学
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- ワクチンウイルスの感染は,ウイルス感染に不可欠なプロセスであるアクチンポリメリゼーションを誘発します.
- このアクチンポリメリゼーションは,Src依存型チロシンリン酸化により,ウイルス膜タンパク質A36Rによって調節されていることが知られている.
研究 の 目的:
- Srcの活性化とA36Rのリン酸化を調節する上流のシグナルイベントを解明する.
- ワクチンウイルスの運動性がマイクロチューブルベースの輸送からアクチンベースの運動性への移行におけるSrc活動の役割を理解する.
主な方法:
- Srcキナーゼの活性化におけるウイルス膜タンパク質B5Rの役割を調査した.
- B5Rのシグナル伝達に反応するA36Rのリン酸化状態を分析した.
- Src媒介によるA36Rリン酸化が,ウイルス粒子による従来のキネシンの徴募と放出に及ぼす影響を調査した.
主要な成果:
- ウイルスのタンパク質B5Rによって開始された局所的な外からの内へのシグナルカスケードは,プラズマ膜での強力なSrc活性化に不可欠です.
- B5R誘発のSrc活性化は,A36Rのチロシンリン酸化につながります.
- Src媒介によるA36Rのリン酸化は,ウイルス粒子が従来のキネシンと相互作用し,その輸送に影響を及ぼします.
結論:
- Srcキナーゼは,ワクチンウイルス運動性の重要な調節剤として作用します.
- B5Rが誘発するシグナル伝達経路は,微小管に依存する細胞質輸送と細胞表面でのアクチンベースの運動性との間の切り替えを制御する.
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