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CALM1 — GRK5
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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
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
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