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	
2.7.11.16	malfunction	over expression of kinase-inactive K215R GRK5 or GRK5 knockdown leads to G2/M arrest in the cell cycle. Loss of GRK5 activity results in decreased cyclin D1 expression, Rb protein phosphorylation and E2F target gene expression involved in cell cycle control	725847	
2.7.11.16	malfunction	silencing of GRK5 by RNA interference attenuates in vitro cell proliferation. Reduced expression of GRK5 goes ahead with reduced xenograft tumor growth in mice	725847	
2.7.11.16	malfunction	transient overexpression of GRK5, but not kinase dead mutant K215R, results in a significant increase in p53 phosphorylation	725394	
2.7.11.16	malfunction	with a sublethal dose of Escherichia coli, GRK5 knockout mice exhibit higher plasma CXCL1/KC levels and enhanced lung neutrophil recruitment early after infection, and lower bacterial loads, than wild type mice. The inflammatory response is also diminished, and resolution of inflammation advanced, in the lungs of GRK5 knockout mice	738372	
2.7.11.16	physiological function	enzyme-histone deacetylase 6 interaction contributes to paclitaxel resistance in cancer cells	761893	
2.7.11.16	physiological function	GRK2 and GRK3 are involved in C3aR (G protein coupled receptors for C3a) desensitization	726276	
2.7.11.16	physiological function	GRK2 inhibits Wnt1-induced activation of a reporter construct and reduces Wnt3a-dependent stabilization and nuclear translocation of beta-catenin,	705737	
2.7.11.16	physiological function	GRK5 and GRK6 promote C3a-induced mast cell degranulation but inhibit ERK1/2 phosphorylation via C3aR desensitization-independent mechanisms	726276	
2.7.11.16	physiological function	GRK5 has an important role in the regulation of prostate tumor growth	725847	
2.7.11.16	physiological function	GRK5 is localized in the centrosome and regulates microtubule nucleation and normal cell cycle progression	725509	
2.7.11.16	physiological function	GRK5 negatively regulates CXCL1/KC levels during bacterial pneumonia	738372	
2.7.11.16	physiological function	GRK5 phosphorylates nucleophosmin and regulates the sensitivity of cells to PLK1 inhibition	725471	
2.7.11.16	physiological function	GRK5 phosphorylates p53 at Thr-55, which promotes the degradation of p53, leading to inhibition of p53-dependent apoptotic response to genotoxic damage	725394	
2.7.11.16	physiological function	isoform GRK6 regulates epithelial-mesenchymal transition phenotypes and matrix metalloproteinase expression. Hypermethylation of the GRK6 gene promoter suppresses binding of CCAAT/enhancer-binding protein-alpha, thereby contributing to the promotion of cell migration and invasion in lung adenocarcinoma	761095	
2.7.11.16	physiological function	the enzyme is probably associated with dendritic formation in post-status epilepticus hippocampus	761015	
2.7.11.16	physiological function	the enzyme plays a role in urotensin II-mediated cellular hypertrophy via activation of nuclear factor-kappaB and histone deacetylase 5	739053	
2.7.11.16	physiological function	the enzyme regulates migration and invasion of prostate cancer cells	737975	
2.7.11.16	physiological function	the RH domain of GRK5 interacts with IkappaBalpha and causes inhibition of NFkappaB activity, GRK5 overexpression causes nuclear accumulation of IkappaBalpha leading to the inhibition of NFkappaB transcriptional activity, the GRK5-RH domain inhibits TNFalpha transcription, inhibits endothelial cell migration, and vascular tube formation	706487