2.7.11.16	malfunction	depletion of endogenous GRK2 enhances canonical signaling	705737	
2.7.11.16	malfunction	enzyme deficiency contributes to the pathogenesis of Alzheimer's disease by influencing the hyperphosphorylation of tau through the activation of glycogen synthase kinase 3beta	761592	
2.7.11.16	malfunction	enzyme dysfunction is associated with congenital heart defects	762419	
2.7.11.16	malfunction	GRK5 or GRK6 knockdown has no effect on C3aR (G protein coupled receptors for C3a) desensitization, but causes a significant decrease in C3a-induced mast cell degranulation. GRK5 or GRK6 knockdown render mast cells more responsive to C3a for ERK1/2 phosphorylation	726276	
2.7.11.16	malfunction	GRK5-depleted cells are more sensitive to undergoing cell death from polo-like kinase 1 (PLK1) inhibition, and this increased susceptibility corresponds to decreased NPM1 phosphorylation. Conversely, cells with higher GRK5 levels exhibit reduced sensitivity to PLK1 inhibition	725471	
2.7.11.16	malfunction	inhibition of vascular smooth muscle GRK2 enhances beta-adrenergic receptor signaling	684355	
2.7.11.16	malfunction	isoform GRK6 knockdown promotes cell migration and invasion in lung adenocarcinoma cells	761095	
2.7.11.16	malfunction	knockdown of GRK2 or GRK3 expression using shRNA causes a more sustained Ca2+ mobilization, attenuated C3aR (G protein coupled receptors for C3a) desensitization, and enhanced degranulation as well as ERK1/2 phosphorylation when compared to shRNA control cells	726276	
2.7.11.16	malfunction	knockdown of GRK5 expression leads to G2/M arrest, characterized by a prolonged G2 phase, which can be rescued by expression of wild type but not catalytically inactive GRK5	725509	
2.7.11.16	malfunction	knockdown of GRK5 in osteosarcoma cells inhibits DNAdamage-induced apoptosis via a p53-mediated mechanism	725394