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CALM3 — GRK5

Text-mined interactions from Literome

Freeman et al., FEBS Lett 2000 : In addition, calcium bound calmodulin and phosphatidylinositol 4,5-bisphosphate ( PIP2 ), two regulators of GRK activity, coordinate with alpha-actinin to modulate substrate specificity of the GRKs
Sallese et al., Biochim Biophys Acta 2000 (Calcium Signaling) : The ubiquitous calcium binding protein calmodulin (CaM) can inhibit GRK5 with a high affinity ( IC ( 50 ) =40-50 nM )
Lao et al., Clin Exp Hypertens 2002 (Hypertension) : Because calmodulin kinase ( CaMK ) can regulate GRK activity, CaMK activity in renal cortical membranes of WKHA and WKHT were studied
Monovich et al., FEBS Lett 2010 : Several kinases have been shown to phosphorylate class IIa HDACs, including calcium/calmodulin dependent protein kinase ( CaMK ), protein kinase D (PKD) and G protein coupled receptor kinase ( GRK )
Gold et al., PloS one 2013 (Hypertrophy) : We report here that GRK5 nuclear accumulation is dependent on Ca ( 2+ ) /calmodulin (CaM) binding to a specific site within the amino terminus of GRK5 and this interaction occurs after selective activation of hypertrophic Gq-coupled receptors
Haga et al., Biochemistry 1997 : These results indicate that Ca2+-calmodulin does not directly interact with the catalytic site of GRK2 but inhibits the kinase activity of GRK2 by interfering with the activation of GRK2 by agonist bound m2 receptors and G protein betagamma subunits
Pronin et al., J Biol Chem 1997 : Calmodulin inhibition of GRK5 is mediated via a reduced ability of the kinase to bind to both receptor and phospholipid
Levay et al., Biochemistry 1998 : While specific mutation within the N-terminal site had no effect on calmodulin mediated inhibition of GRK5 activity, deletion of the C-terminal site attenuated the effect of calmodulin on GRK5, and the simultaneous mutation of both sites rendered the enzyme calmodulin-insensitive