Cdc25細胞サイクルフォスファタゼは,c-myccの標的として使用されます
K Galaktionov1, X Chen, D Beach
1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724, USA.
Nature
|August 8, 1996
まとめ
プロトオンコゲンであるc-mycとMaxは,細胞の成長と死を調節する転写因子を形成する. この因子は,Myc誘発のアポトーシスに不可欠なcdc25A遺伝子を標的にし,cdc25Aをc-mycにおける重要なプレーヤーとして強調しています.
科学分野:
- 分子生物学は分子生物学である.
- 腫瘍学 腫瘍学
- 細胞生物学 細胞生物学
背景:
- プロトオンコゲンc-mycは,マックスと共に転写因子を形成する.
- このMyc/Max複合体は,細胞増殖とアポトーシスに関与する遺伝子を調節する.
- また,原発がん遺伝子であるcdc25Aは,特に成長因子がない場合,アポトーシスにおいて役割を果たします.
研究 の 目的:
- c-mycとcdc25A遺伝子の関係を調査する.
- cdc25AがMyc/Max.の直接的な転写標的であるかどうかを判断する.
- Myc誘発のアポトーシスにおけるcdc25Aの役割を明らかにする.
主な方法:
- cdc25A遺伝子プロモーターに結合するMyc/Maxヘテロダイマーの分析.
- Myc/Max.によるcdc25A転写活性化の評価
- Myc誘発のアポトーシスに対するcdc25Aの要求の評価.
主要な成果:
- Myc/Maxヘテロダイマーは,cdc25A遺伝子内の特定の元素と結合する.
- Myc/Max結合は,cdc25A転写の活性化につながる.
- Mycによって誘発されるアポトーシスは,cdc25Aの存在に依存しています.
結論:
- cdc25Aは,c-myc.の生理学的に重要な転写標的である.
- Myc/Max複合体は,cdc25A発現を直接制御する.
- cdc25Aは,Myc誘発によるアポトーシスを媒介するために不可欠です.
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