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Trends Biochem Sci. 2003 Nov;28(11):573-6.

Rheb fills a GAP between TSC and TOR.

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Department of Cell Biology, Harvard Medical School, Division of Signal Transduction, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Rm 1028, 4 Blackfan Circle, Boston, MA 02115, USA.


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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