雷氏菌
TSC1
TSC2
结节性硬化
小型GTPase
GTP酶
生物
细胞生物学
TOR信号
GTPase激活蛋白
计算生物学
信号转导
mTORC1型
PI3K/AKT/mTOR通路
G蛋白
医学
精神科
作者
Brendan D. Manning,Lewis C. Cantley
标识
DOI:10.1016/j.tibs.2003.09.003
摘要
There has been much interest in determining the molecular and cellular functions of hamartin and tuberin, which are encoded by the genes TSC1 and TSC2 that are mutated in the tuberous sclerosis complex disease. Recently, several laboratories have independently reported a major breakthrough in this field. Together, these genetic, biochemical and cell-biological studies have demonstrated that the tuberin-hamartin complex inhibits target of rapamycin (TOR) signaling by acting as a GTPase-activating protein for the Ras-related small G protein Rheb.
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