Gβγ Counteracts Gαq Signaling upon α1-Adrenergic Receptor Stimulation

Gα12/13-mediated Production of Reactive Oxygen Species Is Critical for Angiotensin Receptor-induced NFAT Activation in Cardiac Fibroblasts

“…Because the NFAT transcriptional activity is maintained by persistent elevation of [Ca 2ϩ ] i and the continuous activation of calcineurin (18), Ang II stimulation should lead to a persistent increase in [Ca 2ϩ ] i for NFAT activation. Our previous report using myoblast cell line H9c2 indicated that expression of CARac increases the basal level of [Ca 2ϩ ] i and activates JNK (38). Because G␣ 12/13 regulates Rac activity, one possible pathway is that G␣ 12/13 -activated Rac increases the basal level of [Ca 2ϩ ] i in cardiac fibroblasts.…”

“…Intracellular Ca 2ϩ Measurement-The intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) of cardiac fibroblasts was determined by the method described previously (38). Briefly, cells (1 ϫ 10 5 ) were plated on a glass-bottom 35-mm dish and loaded with 2.5 M Fura2/AM in the cultured medium at 37°C for 30 min.…”

Kisspeptin-10-Induced Signaling of GPR54 Negatively Regulates Chemotactic Responses Mediated by CXCR4: a Potential Mechanism for the Metastasis Suppressor Activity of Kisspeptins

“…Additional studies showed an opposite effect for Gqcoupled receptors (phosphorylation of Akt and inhibition of apoptosis) and CAMs of Gq (reduction of phosphorylation of Akt and apoptosis; ref. 30). These apparently contradictory observations may be reconciled by a model in which Ghg subunits would activate PI3K and Akt whereas Gaq would inhibit them (30,31), hypothesis supported by the fact that Gaq was shown to interact with PI3K (28).…”

ERK1/2: An Integrator of Signals That Alters Cardiac Homeostasis and Growth

“…There are three studies of note that have pointed out that the active GTP-bound alpha subunit is not the only potential effector of GPCR activation. Although one study was focused on the beta/gamma subunit released by the Gs alpha subunit [89] and the other two focused on that which was released by the Gq alpha subunit [87,90], all three concluded that the released beta/gamma subunit is capable of binding to ERK, modulating its activity. It is lastly worth mentioning proteins that contain regulator of G protein signaling (RGS) domains, which are involved in reducing the effect of GPCR activation.…”