Figure 1: G-protein activation and RGS protein-mediated deactivation cycle.

In response to various agonists, the seven transmembrane GPCR undergoes a conformational change and induces the exchange of GDP to GTP on Gα and dissociation from Gβγ dimer, which, in turn, both activated GTP-Gα and Gβγ dimer regulate downstream effectors. This cycle is terminated by the GAP activity of RGS proteins, which accelerates hydrolysis of GTP to GDP and thus terminates GPCR signaling.