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Results 1 - 10 of 18 > >>
EC Number
General Information
Commentary
Reference
malfunction
depletion of endogenous GRK2 enhances canonical signaling
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; 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
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
malfunction
inhibition of vascular smooth muscle GRK2 enhances beta-adrenergic receptor signaling
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
malfunction
knockdown of GRK5 in osteosarcoma cells inhibits DNAdamage-induced apoptosis via a p53-mediated mechanism; transient overexpression of GRK5, but not kinase dead mutant K215R, results in a significant increase in p53 phosphorylation
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; silencing of GRK5 by RNA interference attenuates in vitro cell proliferation. Reduced expression of GRK5 goes ahead with reduced xenograft tumor growth in mice
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
physiological function
GRK2 and GRK3 are involved in C3aR (G protein coupled receptors for C3a) desensitization; GRK5 and GRK6 promote C3a-induced mast cell degranulation but inhibit ERK1/2 phosphorylation via C3aR desensitization-independent mechanisms
physiological function
GRK2 inhibits Wnt1-induced activation of a reporter construct and reduces Wnt3a-dependent stabilization and nuclear translocation of beta-catenin,
Results 1 - 10 of 18 > >>