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Papers In Press, published online ahead of print May 25, 2006
Cancer Research UK Centre of Cell and Molocular Biology, Institute of Cancer Research, London SW3 6JB
Corresponding Author: Richard.Lamb{at}icr.ac.uk
Gain-of-function mutants of Ras- and Rho-family small GTPases have proven to be important tools in analysingsignalling downstream of these small GTPases. The Ras-related GTPaseRheb has emerged as a key player downstream of TSC1-2 is regulatingsignalling to mTOR effectors of cell growth such as S6K and 4E-BP1. The TSC1-2 tumor suppressor complex has been shown to act as a RhebGAP, converting Rheb from a GTP- to a GDP-bound form. Here we report the identification of a mutant Rheb (S16HRheb) that exhibits gain-of-function properties. S16HRheb exhibits both increased GTP loading in vivo and resistance to TSC1-2. Compared to wild-type Rheb, S16HRheb is more active at promoting the phosphorylation of the mTOR effectors S6K1 and 4E-BP1. Thus S16HRheb will help to identify proximal signalling events downstream of Rheb, and allow potential Rheb-independent functions downstream of TSC1-2 to be investigated.
J. Biol. Chem, 10.1074/jbc.C600028200
Submitted on February 9, 2006
Accepted on May 25, 2006
Hyperactivation of MTOR signalling by a gain-of-function mutant of the RHEB GTPase
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