Signaling pathways: the benefits of good communication

Curr Biol. 2004 Dec 14;14(23):R1005-7. doi: 10.1016/j.cub.2004.11.024.

Abstract

Recent studies show that hyperactivated mTOR, the 'target of rapamycin' that senses nutrient availability in eukaryotic cells, inhibits signaling by insulin receptor substrates. This crosstalk reveals how hyperactivated mTOR may suppress metastasis locally, while causing systemic insulin resistance that can progress to diabetes.

Publication types

  • Review

MeSH terms

  • Animals
  • Enzyme Activation / physiology*
  • GTPase-Activating Proteins / metabolism
  • Humans
  • Insulin Resistance / physiology
  • Models, Biological
  • Mutation / genetics
  • Neoplasm Metastasis / physiopathology*
  • Protein Kinases / metabolism*
  • Proteins / genetics
  • Receptor, Insulin / antagonists & inhibitors*
  • Signal Transduction / physiology*
  • TOR Serine-Threonine Kinases
  • Tuberous Sclerosis / metabolism*
  • Tuberous Sclerosis / physiopathology
  • Tuberous Sclerosis Complex 1 Protein
  • Tumor Suppressor Proteins

Substances

  • GTPase-Activating Proteins
  • Proteins
  • Tuberous Sclerosis Complex 1 Protein
  • Tumor Suppressor Proteins
  • Protein Kinases
  • MTOR protein, human
  • Receptor, Insulin
  • TOR Serine-Threonine Kinases