
Non‐canonical functions of the tuberous sclerosis complex‐Rheb signalling axis
Author(s) -
Neuman Nicole A.,
Henske Elizabeth Petri
Publication year - 2011
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.1002/emmm.201100131
Subject(s) - tsc1 , rheb , tsc2 , tuberous sclerosis , pi3k/akt/mtor pathway , cancer research , lymphangioleiomyomatosis , mtorc1 , biology , sirolimus , small gtpase , microbiology and biotechnology , computational biology , signal transduction , medicine , pathology , biochemistry
The protein products of the tuberous sclerosis complex (TSC) genes, TSC1 and TSC2, form a complex, which inhibits the small G‐protein, Ras homolog enriched in brain (Rheb). The vast majority of research regarding these proteins has focused on mammalian Target of Rapamycin (mTOR), a target of Rheb. Here, we propose that there are clinically relevant functions and targets of TSC1, TSC2 and Rheb, which are independent of mTOR. We present evidence that such non‐canonical functions of the TSC‐Rheb signalling network exist, propose a standard of evidence for these non‐canonical functions, and discuss their potential clinical and therapeutic implications for patients with TSC and lymphangioleiomyomatosis (LAM).