Journal
FEBS LETTERS
Volume 579, Issue 21, Pages 4763-4768Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2005.07.054
Keywords
Rheb; mTOR; TSC2; S6K1; 4E-BP1; RhebL1
Funding
- NIGMS NIH HHS [GM51405] Funding Source: Medline
Ask authors/readers for more resources
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. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available