EC Number   |
General Information |
Reference  |
|---|
   2.7.11.16 | malfunction |
inhibition of vascular smooth muscle GRK2 enhances beta-adrenergic receptor signaling |
684355 |
| 2.7.11.16 | malfunction |
depletion of endogenous GRK2 enhances canonical signaling |
705737 |
| 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 |
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 |
| 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 |
transient overexpression of GRK5, but not kinase dead mutant K215R, results in a significant increase in p53 phosphorylation |
725394 |
| 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 | 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 | physiological function |
GRK5 phosphorylates nucleophosmin and regulates the sensitivity of cells to PLK1 inhibition |
725471 |
| 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 |
