Background of the antigen
Heterotrimeric G protein-mediated signal transduction is a dynamically regulated process with the intensity of signal decreasing over time despite the continued presence of the agonist (1,2). G protein-coupled receptor kinases (GRKs) are activated by activated G protein-coupled receptors, and they function to phosphorylate and inactivate cell surface receptors in the heterotrimeric G protein signaling cascade (3,4). GIT1 (for GRK-interactor 1) and GIT2 are GTPase-activating proteins (GAP) for members of the ADP ribosylation factor (ARF) family of small GTP-binding proteins, which are involved in vesicular trafficking (5,6). GIT1 overexpression results in reduced internalization and resensitization of b2-adrenergic receptor, thus reducing b2-adrenergic receptor signaling (5).
