中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2007, 19(1): 21-
Akt-mTOR的互动与癌症的发生
张 超,章雄文,丁 健*
中国科学院上海药物研究所新药研究国家重点实验室肿瘤药理组, 上海 201203
摘 要: PI3K的下游效应蛋白Akt,在人癌中经常处于高度激活状态。mTOR作为Akt下游的重要效应子在肿瘤发生中扮演重要角色。在PI3K-Akt-mTOR这条信号通路中,Akt所产生的效应受到两个肿瘤抑制基因的负调控:PTEN,处于Akt的上游;TSC1/TSC2,位于AKT的下游和mTOR的上游。新的研究结果表明,当缺少TSC1/TSC2的负性调节时,mTOR则通过两种复合物的平衡移动来反馈抑制Akt活性。利用小鼠遗传学手段研究PTEN和TSC2在癌症发生和进展中的角色,也证明AKT-mTOR的互相作用在癌症发展与治疗中的重要性。
关键词:蛋白激酶B;哺乳动物雷帕霉素靶体蛋白;PTEN;结节性脑硬化复合物1/2
 
Akt-mTOR interplaying and carcinogenesis
ZHANG Chao, ZHANG Xiongwen, DING Jian*
Anti-tumor Pharmacology Branch, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
Abstract: The downstream effector of PI3K, Akt, is often highly-activated in human cancers. mTOR, as the downstream effector of Akt, plays pivotal role in carcinogenesis. In PI3K-Akt-mTOR signaling, Akt is negatively regulated by two tumor suppressors: PTEN, located at upstream of Akt and TSC1/TSC2 complex, lies in downstream of Akt. Latest researches indicated that Akt was regulated by a negative feedback mechanism directed by the balance of two mTOR complexes when TSC1/TSC2 was absent. The investigation of PTEN and TSC2 in carcinogenesis by mouse genetic strategies emphasizes the interplaying of Akt and mTOR in cancer research and treatment. 
Key words: Akt; mTOR; PTEN; TSC1/2
 
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