Rheb Fills a GAP Between TSC and TOR

Trends Biochem Sci. 2003 Nov;28(11):573-6. doi: 10.1016/j.tibs.2003.09.003.

Abstract

There has been much interest in determining the molecular and cellular functions of hamartin and tuberin, which are encoded by the genes TSC1 and TSC2 that are mutated in the tuberous sclerosis complex disease. Recently, several laboratories have independently reported a major breakthrough in this field. Together, these genetic, biochemical and cell-biological studies have demonstrated that the tuberin-hamartin complex inhibits target of rapamycin (TOR) signaling by acting as a GTPase-activating protein for the Ras-related small G protein Rheb.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • GTPase-Activating Proteins
  • Genes, Tumor Suppressor
  • Humans
  • Monomeric GTP-Binding Proteins / metabolism*
  • Neuropeptides / metabolism*
  • Protein Kinases / metabolism*
  • Proteins / metabolism*
  • Ras Homolog Enriched in Brain Protein
  • Repressor Proteins / metabolism*
  • Signal Transduction*
  • TOR Serine-Threonine Kinases
  • Tuberous Sclerosis / metabolism
  • Tuberous Sclerosis Complex 1 Protein
  • Tuberous Sclerosis Complex 2 Protein
  • Tumor Suppressor Proteins

Substances

  • GTPase-Activating Proteins
  • Neuropeptides
  • Proteins
  • RHEB protein, human
  • Ras Homolog Enriched in Brain Protein
  • Repressor Proteins
  • TSC1 protein, human
  • TSC2 protein, human
  • Tuberous Sclerosis Complex 1 Protein
  • Tuberous Sclerosis Complex 2 Protein
  • Tumor Suppressor Proteins
  • Protein Kinases
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Monomeric GTP-Binding Proteins