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1 cannabinoid agonist-induced up-regulation of GRK5.
2 ocytes involving CTGF-mediated regulation of GRK5.
3 eurons are enriched in GRK2, arrestin-3, and GRK5.
4 of wild type but not catalytically inactive GRK5.
5 paBalpha in myocytes inhibited the levels of GRK5.
6 , an inhibitor of IkappaB kinase 2 decreased GRK5.
7 r polymorphisms in ADRB1, ADRB2, ADRA2C, and GRK5.
8 to identify potential nuclear substrates for GRK5.
9 s and provides insight into the functions of GRK5.
10 tyrosine-phosphorylate and thereby activate GRK5.
11 osphorylation of membrane-bound rhodopsin by GRK5.
12 membrane binding domain in the C terminus of GRK5.
13 pression of the G protein receptor kinase 5, GRK5.
14 n and reward effects in mice lacking GRK3 or GRK5.
15 erine 375 that was predominantly mediated by GRK5.
16 on with siRNA, we demonstrated that lowering GRK5/6 abolishes IGF1-mediated ERK and AKT activation, w
18 ems to be the case for the GRK2/3 subfamily, GRK5/6 effectively phosphorylate inactive forms of sever
19 G protein-coupled receptor kinases 5 and 6 (GRK5/6), traditionally known to phosphorylate and desens
20 ate that the beta2AR can signal to ERK via a GRK5/6-beta-arrestin-dependent pathway, which is indepen
23 at, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilitates maladaptive myo
24 Mechanistically, we show that this is due to GRK5 acting, in a non-GPCR manner, as a class II histone
29 ated phosphorylation of GRK5 correlated with GRK5 activity, as assessed by seryl phosphorylation of t
31 the fish homologs of GRK2 and -5, Grk2/3 and Grk5, also have unique, complementary, or competitive ro
32 to a stoichiometry of 0.8 mol phosphate/mol GRK5, an extent approximately 5 times greater than obser
33 or of G-protein signaling homology domain of GRK5 and -6 and identified a peptide inhibitor with pote
36 results suggest that p105 phosphorylation by GRK5 and binding of arrestin-2 negatively regulates LPS-
37 the presence of a membrane binding motif in GRK5 and define the importance of a group of hydrophobic
38 nanomolar IC50 values against both GRK2 and GRK5 and good selectivity against other closely related
39 phate production stimulated by H1HR, whereas GRK5 and GRK6 had lesser effects on H1HR phosphorylation
40 Unlike after TAC, swim-trained transgenic GRK5 and nontransgenic littermate control mice exhibited
41 -regulation of GRK5, but not GRK2; moreover, GRK5 and PDGFRbeta were coordinately up-regulated in SMC
42 hospholipid-dependent autophosphorylation of GRK5 and phosphorylation of membrane-bound rhodopsin by
45 a specific site within the amino terminus of GRK5 and this interaction occurs after selective activat
46 e the mechanism underlying the regulation of GRK5 and to identify the role of GRK5 in the cannabinoid
50 These results reveal that arrestin-2 and GRK5 are important negative regulatory components in TLR
56 ein-coupled receptor kinases 2 (GRK2) and 5 (GRK5) are fundamental regulators of cardiac performance
58 Additionally, we have previously classified GRK5 as a determinant of left-right asymmetry and proper
63 n is analogous to one that can be assumed by GRK5, at least partially explaining the loss in selectiv
64 ls being less sensitive and cells with lower GRK5 being more sensitive to PLK1 inhibitor-induced apop
68 dues by G protein-coupled receptor kinase-5 (GRK5), but mechanisms for GRK5 activation by the PDGFRbe
69 eta activation engendered down-regulation of GRK5, but not GRK2; moreover, GRK5 and PDGFRbeta were co
71 horylation is required for the activation of GRK5 by the PDGFRbeta, but not by the beta(2)-adrenergic
73 r factor of activated T cells (NFAT) because GRK5 causes enhancement of NFAT-mediated hypertrophic ge
76 RK5 revealed a nonsynonymous polymorphism of GRK5, common in African Americans, in which leucine is s
78 ree of PDGFRbeta-mediated phosphorylation of GRK5 correlated with GRK5 activity, as assessed by seryl
79 Altogether, these findings indicate that GRK5 deficiency accelerates beta-amyloidogenic APP proce
81 mer disease (AD), but the mechanism by which GRK5 deficiency may contribute to AD pathogenesis remain
83 h other supporting evidence, we propose that GRK5 deficiency selectively renders BFC neurons more vul
86 embrane G protein-coupled receptor kinase 5 (GRK5) deficiency is linked to Alzheimer disease, yet its
88 decreasing the ISF Abeta in both control and GRK5-deficient APPsw mice, failed to correct the differe
89 y was unaffected in splenocytes derived from GRK5-deficient mice but was increased in splenocytes fro
92 m of hypertrophic stimuli, thus facilitating GRK5-dependent regulation of maladaptive hypertrophy.
94 rotein kinase C, c-Jun N-terminal kinase, or GRK5 did not inhibit the Cmpd101-insensitive component o
95 verexpression of dominant negative mutant of GRK5 (dnGRK5) in a cholinergic neuronal cell line led to
97 female mice, VSM-specific overexpression of GRK5 elevates BP mediated by Gi and, at least in part, b
100 (K215R)GRK6 compared with control and (K215R)GRK5-expressing cells, whereas (K215R)GRK6 expression ha
101 ncreased PDGFRbeta-associated Shp2 activity, GRK5-expressing SMCs demonstrated greater PDGF-induced S
102 lammatory protein-2 (MIP-2) induces GRK2 and GRK5 expression in PMNs through phosphoinositide-3-kinas
104 subsequent to the downregulation of GRK2 and GRK5 expression is a critical determinant of PMN migrati
108 egulates 5-HT2A receptor signaling, enhances GRK5 expression; the phosphorylation of CB2 receptors; a
110 rmine the absolute requirement of endogenous GRK5 for cardiac hypertrophy and HF development after ch
111 gion contained within amino acids 546-565 of GRK5 forms an amphipathic helix, with the key features o
114 Here, we demonstrate that arrestin-2 and GRK5 (G protein-coupled receptor kinase 5), proteins tha
115 NF-kappaB signaling in the regulation of the GRK5 gene and expression of this kinase in cardiomyocyte
116 models with global or cardiomyocyte-specific GRK5 gene deletion to determine the absolute requirement
117 e we report that inactivation of one copy of Grk5 gene in transgenic mice overexpressing beta-amyloid
118 onic SNPs of the G protein-coupled kinase 5 (GRK5) gene were significantly associated with postoperat
121 level of basal BRET2 using beta2AR-Rluc and GRK5-GFP2 that was not diminished by agonist stimulation
122 Arg389>Gly and G-protein receptor kinase 5 (GRK5) Gln41>Leu polymorphisms, which are more prevalent
123 imulated responses more effectively than did GRK5-Gln41 in transfected cells and transgenic mice, and
127 the related dominant-negative kinase (K215R)GRK5 had no effect on M(3) mACh receptor phosphorylation
129 on of G proteinen-coupled receptor kinase-5 (GRK5) has previously been shown to possess nuclear activ
134 report that increased levels and activity of GRK5 in failing myocardium may have unique significance
137 the present study was to examine the role of GRK5 in monomicrobial pulmonary infection by using an in
138 ulator of NF-kappaB, increased the levels of GRK5 in myocytes whereas treatment of cells with N-acety
139 In this study, we investigated the role of GRK5 in physiological, swimming-induced hypertrophy (SIH
143 gulation of GRK5 and to identify the role of GRK5 in the cannabinoid agonist-induced up-regulation an
144 ing bacterial pneumonia but that the role of GRK5 in the clinical outcome in this model is dependent
148 down of G protein-coupled receptor kinase 5 (GRK5) in zebrafish embryos resulted in the quantitation
149 In addition, overexpression of GRK2 and GRK5 increased basal levels of phosphorylation of the GR
150 ch), we found that physiologic expression of GRK5 increased PDGF-promoted PDGFRbeta seryl phosphoryla
153 ations, and computational docking to analyze GRK5 interaction with the beta2-adrenergic receptor (bet
154 cannabinoid agonist-induced up-regulation of GRK5 involves CB2 receptors, beta-arrestin 2, and ERK1/2
157 data suggest that although nuclear-localized GRK5 is a pathological mediator after stress, this nonca
160 artery bypass grafting, genetic variation in GRK5 is associated with postoperative AF despite periope
162 o synaptic membranes, whereas phosphorylated GRK5 is found in plasma membrane and cytosolic fractions
164 Overall, these studies demonstrate that GRK5 is localized in the centrosome and regulates microt
165 tress, this noncanonical nuclear activity of GRK5 is not induced during physiological hypertrophy.
173 ACh release in hippocampal slices from young GRK5 knock-out mice was significantly reduced compared w
174 c degeneration and cognitive decline in aged GRK5 knock-out mice, this nonstructural alteration may b
179 lved, we tested the effect of arrestin-2 and GRK5 knockdown on LPS-stimulated signaling components th
182 in inducing conditioned place preference in GRK5 knockout mice, whereas cocaine conditioned place pr
184 increased sensitivity of cardiomyocytes from GRK5-knockout (KO) mice to beta-adrenergic agonists, pre
185 SII in comparison to ANG, whereas those from GRK5 KO mice did not differ from those from WT mice.
186 n contrast to the reduced bacterial loads in GRK5 KO mice following a sublethal dose, at a lethal dos
192 to beta-adrenergic agonists, pretreatment of GRK5-KO cardiomyocytes with rec-hCTGF, as opposed to car
194 In addition, overexpression of wild type GRK5 leads to hyperphosphorylation of US28 that results
195 interval [CI]: 1.1 to 3.7, p = 0.03) whereas GRK5 Leu41 was associated with improved survival in Afri
196 showed a pharmacogenomic interaction between GRK5-Leu41 and beta-blocker treatment, in which the pres
197 cker treatment, in which the presence of the GRK5-Leu41 polymorphism was associated with decreased mo
198 frican-American subjects with heart failure, GRK5-Leu41 protected against death or cardiac transplant
199 , and, like pharmacological betaAR blockade, GRK5-Leu41 protected against experimental catecholamine-
200 tion of excessive catecholamine signaling by GRK5-Leu41 provides a 'genetic beta-blockade' that impro
202 o undergo apoptosis with cells having higher GRK5 levels being less sensitive and cells with lower GR
203 d that transgenic mice with elevated cardiac GRK5 levels have exaggerated hypertrophy and early heart
205 vent that is absolutely required for nuclear GRK5 localization downstream of hypertrophic stimuli, th
208 ing mechanisms underlying an increase in VSM-GRK5 may have a profound influence on the use and develo
211 GRK5 by the PDGFRbeta enhanced the V(max) of GRK5-mediated peptide phosphorylation, by 3.4-fold, with
212 hosphorylation of GRK5 was not necessary for GRK5-mediated phosphorylation of the beta(2)-adrenergic
214 a model whereby the extreme NH2 terminus of GRK5 mediates phospholipid binding and is required for o
220 inus of GRK5 negating CaM binding attenuates GRK5 movement from the sarcolemma to the nucleus and, im
222 cells expressing a tyrosine-to-phenylalanine GRK5 mutant, and in GRK5 peptide phosphorylation assays.
223 receptor interaction, we generated a pool of GRK5 mutants and then utilized the bioassay to identify
236 of NFATc3 expression in the heart protected GRK5 overexpressing transgenic mice from the exaggerated
237 Transgenic mice with cardiomyocyte-specific GRK5 overexpression activate an NFAT-reporter in mice ba
240 Taken together, our results demonstrate that GRK5 phosphorylates Ser-4 in nucleophosmin and regulates
241 fied amino acid T66 of moesin as a principal GRK5 phosphorylation site and showed that enforcing the
243 The two most widely expressed GRKs (GRK2 and GRK5) play a role in cardiovascular disease and thus rep
244 on of the beta2AR and GRK5, we conclude that GRK5 plays a distinctive role in the phosphorylation of
249 y the N-terminal domain of each protein, and GRK5 primarily phosphorylates NPM1 at Ser-4, a site shar
252 ed CP55940 exposure selectively up-regulates GRK5 proteins in rat PFCx and in a neuronal cell culture
254 ignals, demonstrating that nuclear localized GRK5 regulates gene transcription via a pathway critical
260 3 and the C terminus of the beta2AR with the GRK5 RH bundle subdomain, membrane-binding surface, and
261 involves large conformational changes in the GRK5 RH/catalytic domain interface upon receptor binding
263 rophic gene transcription in the nucleus via GRK5's ability to bind DNA directly without a phosphoryl
265 , an NH2-terminal 14-amino acid peptide from GRK5 selectively inhibited receptor phosphorylation by G
268 at knockdown of GRK2, GRK3, or GRK6, but not GRK5, significantly increased carbachol-mediated calcium
269 a xenograft model of human prostate cancer, GRK5 silencing reduced tumor growth, invasion, and metas
270 nd small interfering RNA (siRNA) knockdown], GRK5 (siRNA knockdown), and beta-arrestin1 (siRNA knockd
274 th conditional, cardiac-specific deletion of GRK5 that also demonstrated similar protection from path
275 r localization as overexpression of a mutant GRK5 that cannot enter the nucleus was devoid of NF-kapp
277 -adrenergic receptor, and that by activating GRK5, the PDGFRbeta triggers its own desensitization.
279 First, in analyzing the 5'-flanking DNA of GRK5, the presence of a potential NF-kappaB binding site
280 s with phenylephrine or angiotensinII causes GRK5 to leave the sarcolemmal membrane and accumulate in
281 ooth muscle (VSM)-specific overexpression of GRK5 to recapitulate a selective aspect of hypertension
282 B plays a critical role in the regulation of GRK5 transcription in myocytes and that this may transla
284 erfering RNAs to selectively target GRK2 and GRK5, two of the primary GRKs expressed in HEK293 cells.
286 osphorylation, it has been demonstrated that GRK5, unlike GRK2, can reside in the nucleus of myocytes
287 tes that a novel pathological consequence of GRK5 up-regulation in the injured and failing heart is t
291 tions and co-localization of the beta2AR and GRK5, we conclude that GRK5 plays a distinctive role in
292 e the function of the NH2-terminal region of GRK5, we generated a deletion mutant lacking residues 2-
294 vels of G protein-coupled receptor kinase 5 (GRK5) were found isoform-selective upregulated in both c
295 co-expression with either wild type GRK2 or GRK5, whereas catalytically inactive forms of these kina
296 demonstrate crosstalk among WIP1, CXCR4 and GRK5, which may be important for the aggressive phenotyp
298 entified two moderately frequent variants in GRK5 with minor allele frequencies <10%, and seven very
300 data has uncovered noncanonical activity of GRK5 within nuclei that plays a key role in pathological
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