RGS proteins provide biochemical control of agonist-evoked [Ca2+]i oscillations

Mol Cell. 2001 Mar;7(3):651-60. doi: 10.1016/s1097-2765(01)00211-8.


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.

Publication types

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

MeSH terms

  • Amino Acid Substitution / genetics
  • Animals
  • Calcium / metabolism*
  • Calcium Signaling* / drug effects
  • Carbachol / pharmacology
  • Cells, Cultured
  • Cholecystokinin / pharmacology
  • Electrophysiology
  • Heterotrimeric GTP-Binding Proteins / agonists*
  • Heterotrimeric GTP-Binding Proteins / metabolism*
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Inositol 1,4,5-Trisphosphate / pharmacology
  • Macromolecular Substances
  • Models, Biological
  • Mutation / genetics
  • Pancreas / cytology
  • Pancreas / drug effects
  • Pancreas / metabolism
  • RGS Proteins / antagonists & inhibitors
  • RGS Proteins / genetics
  • RGS Proteins / metabolism*
  • Rats


  • Macromolecular Substances
  • RGS Proteins
  • Inositol 1,4,5-Trisphosphate
  • Carbachol
  • Cholecystokinin
  • Heterotrimeric GTP-Binding Proteins
  • Calcium