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Analysis of mTOR signaling by the small G‐proteins, Rheb and RhebL1
Author(s) -
Tee Andrew R.,
Blenis John,
Proud Christopher G.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.07.054
Subject(s) - rheb , pi3k/akt/mtor pathway , tsc1 , tsc2 , rptor , small gtpase , microbiology and biotechnology , signal transduction , effector , autophagy , phosphorylation , biology , mtorc1 , cancer research , chemistry , biochemistry , apoptosis
The small G protein Rheb (Ras homologue enriched in brain) is known to promote mammalian target of rapamycin (mTOR) signaling. In this study, we show that Rheb like‐1 protein (RhebL1) rescues mTOR signaling during nutrient withdrawal and that tuberous sclerosis complex‐1 (TSC) and TSC2 impairs RhebL1‐mediated signaling through mTOR. We identify critical residues within the switch I region (N41) and ‘constitutive’ effector (Ec) region (Y/F54 and L56) of Rheb and RhebL1, which are required for their efficient activation of mTOR signaling. Mutation of Rheb and RhebL1 at N41 impaired their interaction with mTOR, which identifies mTOR as a common downstream target of both Rheb and RhebL1.