Luo X, Popov S, Bera A K, Wilkie T M, Muallem S
Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75390, USA.
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.
激动剂诱发的细胞内钙离子浓度（[Ca2+]i）振荡一直被认为是一种反映[Ca2+]i对肌醇三磷酸受体调节作用的生物物理现象。在此我们表明，[Ca2+]i振荡是一种由G蛋白信号调节（RGS）蛋白对Ca2+信号进行调节而产生的生化现象。G蛋白偶联受体诱发的[Ca2+]i振荡需要RGS蛋白的作用。抑制内源性RGS蛋白的作用会通过逐步转变为持续反应来破坏激动剂诱发的[Ca2+]i振荡。基于这些发现以及突变型RGS蛋白和抗RGS蛋白抗体对Ca2+信号的影响，我们提出G蛋白偶联受体复合物中的RGS蛋白对[Ca2+]i振荡提供生化控制。
