Mechanisms of ERK1/2 regulation by seven-transmembrane-domain receptors

Curr Pharm Des. 2006;12(14):1683-702. doi: 10.2174/138161206776873725.

Abstract

Control of cell growth and differentiation has long been a focus of intense research interest, particularly in the context of cancer therapeutics. The evolutionarily-conserved extracellular signal-regulated kinases 1 and 2 (ERK1/2) are serine-threonine kinases that respond to a wide range of mitogens and growth factors to initiate changes in cellular proliferation and differentiation, and are the most important members of the mitogen-activated protein kinase (MAPK) family in terms of seven transmembrane-domain receptor (7TMR)-mediated regulation of mitogenic processes. Regulation of the ERK1/2 signaling cascade by 7TMRs is highly complex and cell type-specific. Recent advances in our knowledge of this effector pathway have revealed that its regulation is at least partly independent of traditional G protein-mediated actions arising from the stimulation of 7TMRs. This review summarizes the current position of our knowledge of ERK1/2 regulation, and illustrates the wealth of potential targets available for the development of new strategies for the treatment of proliferative and other ERK-related disorders.

Publication types

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

MeSH terms

  • Animals
  • Humans
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Protein Tyrosine Phosphatases / metabolism
  • Receptors, Cell Surface / metabolism*
  • Signal Transduction

Substances

  • Receptors, Cell Surface
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Protein Tyrosine Phosphatases