Non-canonical functions of the tuberous sclerosis complex-Rheb signalling axis

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).

• Publication year

  2011

• Venue

  EMBO Molecular Medicine

• Publication date

  2011-04-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/emmm.201100131PMID 21412983PMCID 3377068
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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