Coordinated regulation of Ras-, Rac-, and Ca2+-dependent signaling pathways.
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.
Grunicke
Hans H
HH
Medical University of Innsbruck, Biocenter, Division of Medical Biochemistry, Austria.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D005057:Eukaryotic Cells / Q000378:metabolism; D020662:Guanine Nucleotide Exchange Factors / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000378:metabolism; D006801:Humans; D015398:Signal Transduction; D020744:rac GTP-Binding Proteins / Q000378:metabolism*; D018631:ras Proteins / Q000378:metabolism*
D020662:Guanine Nucleotide Exchange Factors; D006160:Guanosine Triphosphate; D020744:rac GTP-Binding Proteins; D018631:ras Proteins; D002118:Calcium