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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 (zeige GPR34 Proteine) kinase isoform 2. Therefore, G protein-coupled receptor (zeige GPR34 Proteine) 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 (zeige TNF Proteine)-induced wound healing in epithelial cells of the colon; Grk2 appears to inhibit TNFalpha (zeige TNF Proteine)-induced apoptosis; Grk2 inhibits TNFalpha (zeige TNF Proteine)-induced ERK (zeige EPHB2 Proteine) activation by inhibiting generation of reactive oxygen species. Homozygous knockout of Grk2 is embryonically lethal in mice.
GRK2 upregulation causes kappa-opioid receptor (zeige OPRK1 Proteine) 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 (zeige ADRB2 Proteine)-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 (zeige TNF Proteine).
this study shows that astragaloside IV alleviates E. coli-caused peritonitis through modulating GRK2-CXCR2 (zeige CXCR2 Proteine) 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 (zeige GNAQ Proteine)) and interfered with signaling through this G protein. These data support the development of GRK2-based therapeutic approaches to prevent hypertrophy and heart failure.
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 (zeige GRK4 Proteine).
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 (zeige POLG Proteine) and renders the channels insensitive to inhibition by Nedd4-2 (zeige NEDD4L Proteine).
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 (zeige PDGFRB Proteine) (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 (zeige OPRM1 Proteine)
eIF3d (zeige EIF3D Proteine) promotes gallbladder cancer (GBC) progression mainly via eIF3d (zeige EIF3D Proteine)-GRK2-AKT (zeige AKT1 Proteine) axis and it may be used as a prognostic factor. The therapeutic targeting of eIF3d (zeige EIF3D Proteine)-GRK2 axis may be a potential treatment approach for GBC.
KHSV miR (zeige MLXIP Proteine)-K3 activates the GRK2/CXCR2 (zeige CXCR2 Proteine)/AKT (zeige AKT1 Proteine) 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 (zeige GRK5 Proteine), 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 (zeige FLNA Proteine) caused an elevation in RalA (zeige rala Proteine) activity and resulted in selective interference with the normal intracellular trafficking and signaling of D2R (zeige DRD2 Proteine) through GRK2.
Results demonstrate that GPR3 (zeige GPR3 Proteine) 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 (zeige GPR3 Proteine) activity.
GRK2 is negatively related to IGF1R (zeige IGF1R Proteine) and IGF1R (zeige IGF1R Proteine), 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 (zeige TNF Proteine)-induced wound healing in epithelial cells of the colon; GRK2 appears to inhibit TNFalpha (zeige TNF Proteine)-induced apoptosis; GRK2 inhibits TNFalpha (zeige TNF Proteine)-induced ERK (zeige EPHB2 Proteine) activation by inhibiting generation of reactive oxygen species. Homozygous knockout of GRK2 is embryonically lethal in mice.
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