雷氏菌
TSC1
P70-S6激酶1
PI3K/AKT/mTOR通路
TSC2
生物
RPTOR公司
细胞生物学
磷酸化
mTORC1型
GTP酶
小型GTPase
癌症研究
自噬
雷帕霉素的作用靶点
结节性硬化
mTORC2型
GTPase激活蛋白
效应器
信号转导
蛋白激酶B
心理学
精神科
作者
Ken Inoki,Yong Li,Tian Xu,Kun Liang Guan
出处
期刊:Genes & Development
[Cold Spring Harbor Laboratory]
日期:2003-07-17
卷期号:17 (15): 1829-1834
被引量:1659
摘要
Tuberous sclerosis complex (TSC) is a genetic disease caused by mutation in either TSC1 or TSC2. The TSC1 and TSC2 gene products form a functional complex and inhibit phosphorylation of S6K and 4EBP1. These functions of TSC1/TSC2 are likely mediated by mTOR. Here we report that TSC2 is a GTPase-activating protein (GAP) toward Rheb, a Ras family GTPase. Rheb stimulates phosphorylation of S6K and 4EBP1. This function of Rheb is blocked by rapamycin and dominant-negative mTOR. Rheb stimulates the phosphorylation of mTOR and plays an essential role in regulation of S6K and 4EBP1 in response to nutrients and cellular energy status. Our data demonstrate that Rheb acts downstream of TSC1/TSC2 and upstream of mTOR to regulate cell growth.
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