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Human Polyclonal ADRBK1 Primary Antibody pour IHC (p), WB - ABIN1882061
Eichmann, Lorenz, Hoffmann, Brockmann, Krasel, Lohse, Quitterer: The amino-terminal domain of G-protein-coupled receptor kinase 2 is a regulatory Gbeta gamma binding site. dans The Journal of biological chemistry 2003
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Human Monoclonal ADRBK1 Primary Antibody pour ICC, IHC - ABIN969178
Chen, Long, Wu, Jiang, Ma: EGF transregulates opioid receptors through EGFR-mediated GRK2 phosphorylation and activation. dans Molecular biology of the cell 2008
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Human Monoclonal ADRBK1 Primary Antibody pour IF, IHC - ABIN966226
Sterne-Marr, Leahey, Bresee, Dickson, Ho, Ragusa, Donnelly, Amie, Krywy, Brookins-Danz, Orakwue, Carr, Yoshino-Koh, Li, Tesmer: GRK2 activation by receptors: role of the kinase large lobe and carboxyl-terminal tail. dans Biochemistry 2009
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Dog (Canine) Polyclonal ADRBK1 Primary Antibody pour ELISA, WB - ABIN547624
Iaccarino, Barbato, Cipolletta, De Amicis, Margulies, Leosco, Trimarco, Koch: Elevated myocardial and lymphocyte GRK2 expression and activity in human heart failure. dans European heart journal 2005
Cow (Bovine) Monoclonal ADRBK1 Primary Antibody pour IHC (fro), IF - ABIN534096
Pitcher, Freedman, Lefkowitz: G protein-coupled receptor kinases. dans Annual review of biochemistry 1998
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FSH enhances CRTC2-mediated gluconeogenesis dependent on AMPK Ser485 phosphorylation via GRK2 in the liver, suggesting an essential role of FSH in the pathogenesis of fasting hyperglycaemia
High GRK2 expression is associated with pulmonary vasoconstrictive disorders.
Enhanced GRK2 expression triggers cardiac hypertrophy by GRK2-PI3Kgamma mediated Akt phosphorylation and subsequent inactivation of GSK3beta.
Grk2 rescuing activity requires the integrity of domains essential for its interaction with GPCRs, we speculate that Grk2 may regulate Hh pathway activity by downregulation of a GPCR.
The main novelty presented here is to show that septic shock induces cardiac hyporesponsiveness to isoproterenol by a mechanism dependent on nitric oxide and mediated by G protein-coupled receptor kinase isoform 2. Therefore, G protein-coupled receptor kinase isoform 2 inhibition may be a potential therapeutic target in sepsis-induced cardiac dysfunction.
Data, including data from studies in heterozygous knockout mice, suggest that Grk2 is involved in TNFalpha-induced wound healing in epithelial cells of the colon; Grk2 appears to inhibit TNFalpha-induced apoptosis; Grk2 inhibits TNFalpha-induced ERK activation by inhibiting generation of reactive oxygen species. Homozygous knockout of Grk2 is embryonically lethal in mice.
GRK2 upregulation causes kappa-opioid receptor desensitization in diabetic heart
study provides the first insights into the role of GRK2 in skeletal muscle physiology and points to a role for GRK2 as a modulator of contractile properties in skeletal muscle as well as beta2AR-induced hypertrophy.
GRK2 loss confers a protective advantage over control mice after myocardial ischemia/reperfusion injury. Fibroblast GRK2 knockout mice presented with decreased infarct size and preserved cardiac function 24 hours post ischemia/reperfusion. They had decreased fibrosis and fibrotic gene expression. These protective effects correlated with decreased infiltration of neutrophils to the ischemia site and decreased TNF-alpha.
this study shows that astragaloside IV alleviates E. coli-caused peritonitis through modulating GRK2-CXCR2 signal in neutrophils
GRK2 down-regulation is cardioprotective during diet-induced obesity, reinforcing the protective effect of maintaining low levels of GRK2 under nutritional stress, and showing a role for this kinase in obesity-induced cardiac remodeling and steatosis.
The betaARKrgs peptide, but not endogenous GRK2, interacted with Galpha(q) and interfered with signaling through this G protein. These data support the development of GRK2-based therapeutic approaches to prevent hypertrophy and heart failure.
GRK2 is localized in the mitochondria and its kinase activity negatively impacts the function of this organelle by increasing superoxide levels and altering substrate utilization for energy production.
Erythropoietin seems to reverse sepsis-induced vasoplegia to NE through the preservation of alpha1D adrenoceptor mRNA/protein expression, inhibition of GRK2-mediated desensitization, and attenuation of NO overproduction in the mouse aorta.
In vitro, GRK2 inhibits Epac1-to-Rap1 signaling by phosphorylation of Epac1 at Ser-108 in the Disheveled/Egl-10/pleckstrin domain. GRK2 inhibits Epac1-mediated sensitization of Piezo2 which contributes to inflammatory mechanical hyperalgesia.
GRK2 ablation increases circadian amplitude and decreases circadian period. GRK2 suppresses mPeriod1 transcription,PERIOD1/2 nuclear trafficking and promotes PERIOD2 phosphorylation.
These results suggest GRK2 contributes to melanopsin deactivation, but that other mechanisms account for most of modulation of melanopsin activity in ipRGCs.
data suggest that inhibiting GRK2 could reverse an established insulin-resistant and obese phenotype
Post-MI AdipoR1 phosphorylation positively correlated with the expression level of GRK2. AdipoR1 is phosphorylatively modified and desensitized by GRK2 in failing cardiomyocytes, contributing to post-MI remodeling and HF progression.
findings indicate that the balance between mechanisms regulating vascular tone are shifted to favor vasoconstriction in the absence of GRK2 expression and that this leads to the age-dependent development of hypertension
The PIP2-induced orientation of the GRK2-Gbeta1gamma2 complex is therefore most likely caused by specific interactions between PIP2 and the GRK2 PH domain.
Mitochondrial-targeted GRK2 is essential for prodeath signaling occurring after oxidative stress in myocytes and assigning a novel role for this GRK.
Indicate that the anti-proliferative function of elevated GRK2 in hepatocellular carcinoma is associated with delayed cell cycle progression and is GRK2 kinase activity-dependent.
G alpha q/11 interacts with this protein. A novel surface on a regulator of G protein signals a homology domain for binding G alpha subunits (GRK2 kinase}
determined the crystallographic structure of GRK2 in complex with G protein beta1gamma2 subunits.
intramolecular interactions could play a role in regulating G protein-coupled receptor kinase 2 (GRK2).
epithelial Na-channels are maintained in the active state by Grk2; Grk2 phosphorylates the C terminus of the channel beta subunit and renders the channels insensitive to inhibition by Nedd4-2.
Crystallographic and biochemical studies provide evidence that the major domain interfaces of G protein-coupled beta adrenergic receptor kinase 1 (GRK2) remain associated during Gbetagamma binding and activation of GRK2.
Resultrs suggest that activated platelet-derived growth factor receptor-beta (PDGFRbeta) phosphorylates GRK2 tyrosyl residues and thereby activates GRK2, which then serine-phosphorylates and desensitizes the PDGFRbeta.
GRK2-as5 has a role in membrane trafficking of the mu-opioid receptor
atomic structure of GRK2 in complex with Galphaq and Gbetagamma, in which activated Galpha subunit of Gq is fully dissociated from Gbetagamma and dramatically reoriented from its position in the inactive Galphabetagamma heterotrimer [Galphaq, Gbetagamma
G protein-coupled receptor kinase 2 plays a positive role in Smoothened signaling, at least in part, through the promotion of an association between beta-arrestin 2 and Smoothened
results reveal that the D2R can directly recruit GRK2 without G protein activation and that this mechanism may have relevance to achieving betaarr-biased signaling
M3R activation-induced GRK2 recruitment is Ggamma subtype dependent in which Gbetagamma dimers with low cell membrane-affinity Ggamma9 exhibited a two-fold higher GRK2-recruitment compared to high affinity Ggamma3 expressing cells.
Chronic/pathologic GPCR signaling elicits the interaction of the G-protein Gbetagamma subunit with GPCR kinase 2 (GRK2), targeting the receptor for internalization, scaffolding to pathologic signals, and receptor degradation. Targeting this pathologic Gbetagamma-GRK2 interaction has been suggested as a possible strategy for the treatment of HF.
A novel regulatory role of GRK2 was proposed for the ubiquitination of beta-arrestin in the context of the PKC-mediated heterologous regulation of GPCRs.
eIF3d promotes gallbladder cancer (GBC) progression mainly via eIF3d-GRK2-AKT axis and it may be used as a prognostic factor. The therapeutic targeting of eIF3d-GRK2 axis may be a potential treatment approach for GBC.
KHSV miR-K3 activates the GRK2/CXCR2/AKT axis inducing KSHV-induced angiogenesis and promoting KSHV latency.
Compared to the original peptide, a modified peptide (Ac-EEMEFSEAEANMN-NH2) exhibited markedly higher affinity for GRK2, but very low affinity for GRK5, suggesting that it can be a sensitive and selective peptide for GRK2
Low grk2 expression is associated with lung metastasis in gastric cancer.
Lowering the level of cellular FLNA caused an elevation in RalA activity and resulted in selective interference with the normal intracellular trafficking and signaling of D2R through GRK2.
Results demonstrate that GPR3 signals at the plasma membrane and can be silenced by GRK2/beta-arrestin overexpression. These results also strongly implicate the serine and/or threonine residues in the third intracellular loop in the regulation of GPR3 activity.
GRK2 is negatively related to IGF1R and IGF1R, but not GRK2, was associated with the tumour-node-metastasis stage and overall and disease-free survival in hepatocellular carcinoma.
The tyrosine-phosphorylated GRK2 mediates this inhibition by acting on the second intracellular loop of D3R.
GRK2 is overexpressed in pancreatic cancer, and might serve as a potential indicator of unfavorable prognosis.
Data, including data from studies in heterozygous knockout mice, suggest that GRK2 is involved in TNFalpha-induced wound healing in epithelial cells of the colon; GRK2 appears to inhibit TNFalpha-induced apoptosis; GRK2 inhibits TNFalpha-induced ERK activation by inhibiting generation of reactive oxygen species. Homozygous knockout of GRK2 is embryonically lethal in mice.
The dominant model (CC vs. CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese.
Our data suggest that GRK2 acts as an important onco-modulator by strengthening the functionality of key players in breast tumorigenesis such as HDAC6 and Pin1.
GRK2 may inhibit IGF1-induced human hepatocellular carcinoma cell growth and migration through downregulation of EGR1.
It is a critical factor in diabetic endothelial dysfunction and plays a role in many physiological functions including regulation of G-protein-coupled receptors (GPCRs). (review)
Suggest a common regulatory pattern for the beta(2)-AR/GRK2 which is independent of cellular type or pathology.
The product of this gene phosphorylates the beta-2-adrenergic receptor and appears to mediate agonist-specific desensitization observed at high agonist concentrations. This protein is an ubiquitous cytosolic enzyme that specifically phosphorylates the activated form of the beta-adrenergic and related G-protein-coupled receptors. Abnormal coupling of beta-adrenergic receptor to G protein is involved in the pathogenesis of the failing heart.
beta-adrenergic receptor kinase 1
, adrenergic, beta, receptor kinase 1
, G-protein-coupled receptor kinase 2
, beta ARK
, beta ARK1
, beta-AR kinase-1
, beta-adrenergic receptor kinase-1
, G-protein coupled receptor kinase 2
, adrenergic receptor kinase, beta 1
, beta-adrenergic receptor kinase 1 beta ARK1