RGS8 accelerates G-protein-mediated modulation of K + currents

摘要: Transmembrane signal transduction via heterotrimeric G proteins is reported to be inhibited by RGS (regulators of G-protein signalling) proteins1,2,3,4. These work increasing the GTPase activity protein α-subunits (Gα), thereby driving into their inactive GDP-bound form5,6,7. However, it not known how regulate kinetics physiological responses that depend on proteins. Here we report isolation a full-length complementary DNA encoding neural-tissue-specific protein, RGS8, and determination its function. We show RGS8 binds preferentially Gαo Gαi3 functions as GTPase-activating (GAP). When co-expressed in Xenopus oocytes with G-protein-coupled receptor inwardly rectifying K+channel (GIRK1/2), accelerated only turning off but also GIRK1/2 current upon stimulation, without affecting dose–response relationship. conclude accelerates modulation channels just simple negative regulator. This property may crucial for rapid regulation neuronal excitability stimulation receptors.