ルース・サルコマウイルスは,変容を誘導することなく,ミリスティック酸の欠乏したタンパク質を変換し,既知のポリペプチド基板をミリスティック酸リン酸化物で変換します
Cell
|April 11, 1986
まとめ
Rous サルコマウイルスの変形タンパク質であるp60srcの変異は,膜結合を防ぐが,キナーゼ活性を維持する. これは,単にキナーゼ活動ではなく,膜に関連したタンパク質のリン酸化が,細胞の変容に不可欠であることを示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 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
背景:
- ルース・サルコマウイルス (RSV) は,そのp60srcタンパク質を通じて細胞を変容させます.
- p60srcはチロシンタンパク質キナーゼ活性を持ち,膜結合のためにミリスチル化が必要です.
研究 の 目的:
- RSV誘発の細胞変異におけるp60srcミリスチル化と膜局所化の役割を調査する.
- p60srcキナーゼ活性,基板リン酸化,および細胞変容フェノタイプ間の相関を決定する.
主な方法:
- ミュタントのp60srcタンパク質が生成され,ミリスチル化と膜結合が欠けています.
- 変異したRSVに感染した細胞と,細胞タンパク質のチロシンリン酸化を分析した.
- アンカレーズ独立成長,細胞骨格組織,およびフィブロネクチン/プロテアゼ分泌を含む評価された細胞フェノタイプ.
主要な成果:
- 変異したp60srcはチロシンタンパク質キナーゼの活性を維持したが,細胞を変換することはできなかった.
- 変異に関連する細胞現象型は,変異ウイルスによって誘発されませんでした.
- 既知のp60src基板の広範なチロシンリン酸化が発生し,野生型の変形細胞と定量的に異なった.
結論:
- ミリスチル化とp60srcの膜局所化は,Rousの肉腫ウイルスが誘発する細胞変異に不可欠です.
- 特定の膜関連タンパク質のリン酸化は,まだ特定されていないが,おそらく変換に不可欠である.
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