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Updated: Jul 6, 2026

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RhoC GTPase Activation Assay
Published on: August 22, 2010
Ha-Rasとの腫瘍的および転写的協力には,c-Junのセルリン63および73のリン酸化が必要です
T Smeal1, B Binetruy, D A Mercola
1Department of Pharmacology, University of California San Diego, School of Medicine, La Jolla 92093-0636.
Nature
|December 12, 1991
まとめ
腫瘍性Ha-rasシグナリングは,c-Junをセルリン63と73でリン酸化することによってAP-1複合体を活性化させます. このリン酸化は,Ha-ras誘発の細胞変異と遺伝子発現の変化に不可欠です.
科学分野:
- 分子生物学は分子生物学である.
- セルラー・シグナリング
- 腫瘍学 腫瘍学
背景:
- 腫瘍プロモーター,トランスフォーメーション,アクティベータータンパク質-1 (AP-1) の活性が関連しています.
- タンパク質キナーゼCの活性化と成長因子は,AP-1のDNA結合活動を刺激する.
- JunとFosタンパク質で構成されるAP-1複合体は,シグナリングカスケードの中心にある.
研究 の 目的:
- 腫瘍性シグナル伝達における標的としてのc-Junの役割を調査する.
- Ha-rasがc-Junの活動と変容にどのように影響するか解明する.
- Ha-ras.によって規制されたc-Junの特定のリン酸化部位をマッピングする.
主な方法:
- タンパク質キナーゼCの活性化とそのAP-1DNA結合への影響について研究した.
- ラットの胚性線維芽細胞をc-JunとHa-rasを用いた変換アッセイに利用した.
- c-Jun.でリン酸化部位を特定および分析するために,サイト指向型変異を生成した.
主要な成果:
- 線維芽細胞の腫瘍学的変異には,機能的なc-Jun転写活動が必要です.
- 腫瘍性Ha-rasの発現はc-Junのトランザクティベーションを高め,そのリン酸化を刺激する.
- c-Junのリン酸化部位,特にセリン63と73は,Ha-ras反応性としてマッピングされました.
結論:
- Ha-rasによるc-Junのセルリン63と73でのリン酸化は,その活性化に不可欠である.
- このリン酸化は,がん性変異において,Ha-rasがc-Junとの協力に不可欠である.
- c-Junは重要なメディエーターとして作用し,腫瘍性シグナリングを変異のための変異遺伝子発現に変換します.
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