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EPHB2 — GRK5
Text-mined interactions from Literome
Kurose et al., Nihon Yakurigaku Zasshi 1999
(Myocardial Reperfusion Injury) :
Expression of
GRK2-ct inhibited the H2O2 induced activation of
ERK by 70 % and also inhibited the activation of Akt by 30 % ... In contrast with H2O2 induced activation of
ERK , the activation of ERK induced by phorbol ester PMA and the activation of JNK and p38 induced by H2O2 were not
affected by expression of
GRK2-ct , indicating that the activation of ERK but not JNK and p38 is dependent on beta gamma subunit
Thakker et al., Neuropharmacology 2002
(Neuroblastoma) :
Protein kinase C ( PKC ), but not
ERK1/2 , inhibition
blocked OFQ/N mediated
GRK3 induction and mu and ORL1 receptor desensitization in BE ( 2 ) -C cells ... Here, we demonstrate for the first time a role for
ERK1/2 mediated
GRK2 induction in the development of tolerance to mu agonists, as well as cross-tolerance to OFQ/N ... We also demonstrate that chronic OFQ/N mediated desensitization of ORL1 and mu receptors occurs via cell-specific pathways, involving
ERK1/2 dependent
GRK2 , or PKC dependent and ERK1/2 independent GRK3 induction
Ren et al., Proc Natl Acad Sci U S A 2005
:
GRK2 suppression actually
increased beta-arrestin stimulated
ERK activation
Kim et al., Proc Natl Acad Sci U S A 2005
:
Consistent with these findings, beta-arrestin mediated
ERK activation is
enhanced by overexpression of
GRK 5 and 6, and reciprocally diminished by GRK 2 and 3
Gao et al., Acta Biochim Biophys Sin (Shanghai) 2005
(MAP Kinase Signaling System) :
Western blotting assay shows that EGF induced ERK/MAPK phosphorylation increases 1.9-fold, 1.1-fold and 1.5-fold ( P < 0.05 ) at time point 30, 60 and 120 min, respectively when the cells were transfected with GRK2, suggesting the regulatory
role of
GRK2 on EGF induced
ERK/MAPK activation
Jiménez-Sainz et al., Mol Biol Cell 2006
:
This effect is independent of its role in receptor phosphorylation because the kinase-deficient mutant GRK2K220R was able to reduce this response, and
ERK activation by CCR2BIX, a phosphorylation-defective receptor mutant, was also
inhibited by
GRK2 ... These results suggest an important
role for
GRK2 in the control of chemokine induction of
ERK activation at the level of the MEK-ERK interface
Shenoy et al., J Biol Chem 2006
:
Interestingly, overexpression of
GRK5 or -6 increased mutant receptor phosphorylation and beta-arrestin recruitment, led to the formation of stable receptor-beta-arrestin complexes on endosomes, and
increased agonist stimulated
phospho-ERK1/2
Kara et al., Mol Endocrinol 2006
:
G protein coupled receptor kinase 5 ( GRK5 ) and GRK6 were
required for beta-arrestin dependent
ERK activation by both the wild-type and 5A FSH-R ... In conclusion, we demonstrate the existence of a beta-arrestin
dependent ,
GRK regulated mechanism for
ERK activation by the FSH-R
Parameswaran et al., J Biol Chem 2006
:
Arrestin-2 and
G protein coupled receptor kinase 5 interact with NFkappaB1 p105 and negatively
regulate lipopolysaccharide stimulated
ERK1/2 activation in macrophages
Salim et al., FEBS Lett 2007
:
Activation of the CRF ( 1 ) receptor causes
ERK1/2 mediated increase in
GRK3 expression in CATH.a cells
Kleibeuker et al., J Neurochem 2008
:
Conversely, the 45 % decrease in
GRK2 expression in astrocytes from GRK2+/- animals
resulted in a more pronounced CCL2 induced
ERK1/2 phosphorylation ... We found that
GRK2 kinase activity was not
required to decrease chemokine induced
ERK1/2 phosphorylation, whereas regulation of CCL2 induced Akt phosphorylation did require an active GRK2 kinase domain
Lee et al., Br J Nutr 2010
:
The extracellular signal regulated protein kinase 1/2 ( ERK1/2 ) -connexin 43 (Cx43) signalling pathway is crucial for the regulation of GJIC, and both GOK and
GRK blocked the H2O2 induced phosphorylation of Cx43 and
ERK1/2 in WB-F344 cells
Guo et al., PloS one 2011
:
Silencing
GRK2 or GRK3 expression caused a more sustained Ca ( 2+ ) mobilization, attenuated C3aR desensitization, and
enhanced degranulation as well as
ERK1/2 phosphorylation when compared to shRNA control cells ... Furthermore, it reveals the novel finding that
GRK5 and GRK6 promote C3a induced mast cell degranulation but
inhibit ERK1/2 phosphorylation via C3aR desensitization independent mechanisms
Liu et al., Nat Immunol 2012
:
The extracellular signal regulated kinase
Erk potentiated activity of the G protein coupled receptor kinase
GRK2 and inhibited neutrophil migration, whereas the MAPK p38 acted as a noncanonical GRK that phosphorylated the formyl peptide receptor FPR1 and facilitated neutrophil migration by blocking GRK2 function
Zheng et al., Proc Natl Acad Sci U S A 2012
:
By suppressing GRK expression with siRNA, we demonstrated that lowering GRK5/6 abolishes IGF1 mediated
ERK and AKT activation, whereas
GRK2 inhibition
increases ERK activation and partially inhibits AKT signaling
Zhang et al., J Biol Chem 2012
:
We also found that nociceptin induced NOPR mediated JNK but not
ERK signaling
requires Ser-363,
GRK3 , and Arrestin3