RGS proteins provide biochemical control of agonist-evoked [Ca2+]i oscillations.
Agonist-evoked [Ca2+]i oscillations have been considered a biophysical phenomenon reflecting the regulation of the IP3 receptor by [Ca2+]i. Here we show that [Ca2+]i oscillations are a biochemical phenomenon emanating from regulation of Ca2+ signaling by the regulators of G protein signaling (RGS) proteins. [Ca2+]i oscillations evoked by G protein-coupled receptors require the action of RGS proteins. Inhibition of endogenous RGS protein action disrupted agonist-evoked [Ca2+]i oscillations by a stepwise conversion to a sustained response. Based on these findings and the effect of mutant RGS proteins and anti-RGS protein antibodies on Ca2+ signaling, we propose that RGS proteins within the G protein-coupled receptor complexes provide a biochemical control of [Ca2+]i oscillations.
Luo
X
X
Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75390, USA.
Popov
S
S
Bera
A K
AK
Wilkie
T M
TM
Muallem
S
S
D019943:Amino Acid Substitution / Q000235:genetics; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology; D002478:Cells, Cultured; D002766:Cholecystokinin / Q000494:pharmacology; D004594:Electrophysiology; D020962:Heterotrimeric GTP-Binding Proteins / Q000819:agonists* / Q000378:metabolism*; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism / Q000494:pharmacology; D046911:Macromolecular Substances; D008954:Models, Biological; D009154:Mutation / Q000235:genetics; D010179:Pancreas / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D020710:RGS Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D051381:Rats
D046911:Macromolecular Substances; D020710:RGS Proteins; D015544:Inositol 1,4,5-Trisphosphate; D002217:Carbachol; D002766:Cholecystokinin; D020962:Heterotrimeric GTP-Binding Proteins; D002118:Calcium