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通过PI(3)K和PKB传递Ras信号来抑制c-Myc诱导的亡
A Kauffmann-Zeh1, P Rodriguez-Viciana, E Ulrich
1Imperial Cancer Research Fund, London, UK.
拉斯信号激活了相互矛盾的途径,通过酸-3-酶 (PI(3) K) 和蛋白酶B/Akt抑制c-Myc诱导的亡,但通过Raf途径促进亡.
科学领域:
- 细胞生物学 细胞生物学
- 分子瘤学分子瘤学
- 信号传导是指信号的传导方式.
背景情况:
- 细胞活力依赖于抑制细胞亡的生存因素,这是一个被编程的细胞死亡过程.
- 抗亡途径的缺陷与癌症等病理有关,瘤细胞必须逃避亡.
- 酸丁醇-3-酶 (PI(3) K) 对于细胞内信号转导和生存信号发送至关重要.
研究的目的:
- 研究PI(3) K,Ras,PKB/Akt和p70S6K在调节由蛋白c-Myc.诱导的亡中的作用.
- 阐明Ras在通过不同的信号通路调节细胞活力的双重作用.
主要方法:
- 通过c-Myc.诱导纤维细胞亡.
- 对Ras,PI(3)K,PKB/Akt和p70S6K信号通路的分析.
- 评估细胞活力和细胞亡调节.
主要成果:
- 拉斯激活PI(3) K通过激活PKB/Akt来抑制c-Myc诱导的亡,但不是p70S6K.
- 拉斯还通过Raf途径促进细胞亡,表明有矛盾的信号传递.
- 拉斯激活PI(3) K和PKB/Akt对于抑制c-Myc诱导的亡至关重要.
结论:
- 拉斯在细胞活力中表现出双重作用,能够抑制和促进细胞亡.
- PI(3) K/PKB/Akt通路是Ras-依赖的抑制c-Myc诱导的亡的关键调解者.
- 拉斯诱导的亡可能会限制患有瘤性拉斯突变的体细胞的增殖.
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