Rheb fills a GAP between TSC and TOR
Rheb fills a GAP between TSC and TOR
复制标题
DOI：
10.1016/j.tibs.2003.09.003
复制
发表时间：
2003-11-01
影响因子：
13.8
通讯作者：
Cantley, LC
中科院分区：
文献类型：
--
作者：
Manning, BD;Cantley, LC
在结节性硬化症中，由TSC1和TSC2基因编码的错构体和tuberin的分子和细胞功能已经引起了很大的兴趣。最近，几个实验室独立报告了这一领域的重大突破。总之，这些遗传、生化和细胞生物学研究表明，tuberin- hamatin复合物通过作为ras相关小G蛋白Rheb的gtpase激活蛋白抑制雷帕霉素（TOR）信号传导的靶标。
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.