Rheb fills a GAP between TSC and TOR

被引：391

作者：

Manning, BD ^{[1
]}

Cantley, LC ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dept Cell Biol,Harvard Inst Med, Div Signal Transduct,Beth Israel Deaconess Med Ct, Boston, MA 02115 USA

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2003年 / 28卷 / 11期

关键词：

D O I：

10.1016/j.tibs.2003.09.003

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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.

引用

页码：573 / 576

页数：4

共 25 条

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