Coordinated regulation of Ras-, Rac-, and Ca2+-dependent signaling pathways

Crit Rev Eukaryot Gene Expr. 2009;19(2):139-69. doi: 10.1615/critreveukargeneexpr.v19.i2.40.

Abstract

Stimulation of cells by a broad variety of agonists results in a coordinated activation of Ca2+-, Ras-, and Rac-dependent pathways, which have to synergize to yield the corresponding biological response. This synergy requires a dense net of mutually positive and negative regulatory mechanisms. These include Ca2+-mediated activation of guanine nucleotide exchange proteins, resulting in increased levels of GTP-charged Ras and/or Rac or inactivation of small GTPases by Ca2+-mediated activation of GTPase-activating enzymes. Likewise, Ras as well as Rac control regulatory mechanisms, resulting in increased or diminished levels of cytosolic-free Ca2+. The biochemical mechanisms underlying these effects are discussed, with special reference to regulation of Ca2+ signaling by Ras and Rac.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Signaling
  • Eukaryotic Cells / metabolism
  • Guanine Nucleotide Exchange Factors / metabolism
  • Guanosine Triphosphate / metabolism
  • Humans
  • Signal Transduction*
  • rac GTP-Binding Proteins / metabolism*
  • ras Proteins / metabolism*

Substances

  • Guanine Nucleotide Exchange Factors
  • Guanosine Triphosphate
  • rac GTP-Binding Proteins
  • ras Proteins
  • Calcium