EC Number   |
General Information |
Reference |
|---|
   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 |
