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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Adrenergic, beta, receptor kinase 1

GRK2, beta-adrenergic receptor kinase, betaARK1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: V1a, CAN, IRBP, GPCR, GRK5
Papers using GRK2 antibodies
EGF transregulates opioid receptors through EGFR-mediated GRK2 phosphorylation and activation
Hess Sonja, In PLoS ONE, 2007
... Rabbit anti-DDB2 antibody, rabbit anti-GRK2 antibody, and protein A/G agarose were from Santa Cruz Biotechnology.
Protein kinase signaling in the modulation of microvascular permeability
Mehta Dolly et al., In The Journal of Experimental Medicine, 2001
... Anti-FAK, anti–phospho FAK PY576, anti-RhoA, anti-RACK1, anti-Gβ1, anti-Fyn, anti-cSrc, anti-VE-cadherin, anti-GRK2, anti-GFP, anti-p120, anti-phosphotyrosine Abs (PY20, PY99, and PY350), and protein A/G agarose beads were purchased from Santa Cruz Biotechnology, Inc ...
Papers on GRK2
G protein-coupled receptor kinase-2 in peripheral blood mononuclear cells following acute mental stress.
Acevedo et al., Virginia, South Africa. In Life Sci, Jan 2016
AIMS: This study investigated G-protein-coupled receptor kinase-2 (GRK2) density in peripheral blood mononuclear cells (PBMC) and its relationship to plasma pro-inflammatory cytokine concentrations following acute mental stress.
Inhibition of G-protein-coupled receptor kinase 2 prevents the dysfunctional cardiac substrate metabolism in fatty acid synthase-transgenic mice.
Quitterer et al., Zürich, Switzerland. In J Biol Chem, Jan 2016
Here we investigated whether inhibition of G-protein-coupled receptor kinase 2 (GRK2) could counteract the disturbed substrate metabolism of late-stage heart failure.
Endothelin-1 suppresses insulin-stimulated Akt phosphorylation and glucose uptake via G protein-coupled receptor kinase 2 in skeletal muscle cells.
Miwa et al., Sapporo, Japan. In Br J Pharmacol, Jan 2016
C-terminus region of G protein-coupled receptor kinase 2 (GRK2-ct), a dominant negative GRK2, was overexpressed in L6 cells using adenovirus-mediated gene transfer.
Molecular physiopathology of obesity-related diseases: multi-organ integration by GRK2.
Vila-Bedmar et al., Madrid, Spain. In Arch Physiol Biochem, Dec 2015
In particular, we focus on the importance of studying the integrated regulation of different organs and pathways that contribute to the global pathophysiology of this condition with a specific emphasis on the role of emerging key molecular nodes such as the G protein-coupled receptor kinase 2 (GRK2) signalling hub.
Cholesterol-rich lipid rafts are involved in Neuropeptide FF anti-Nociceptin/Orphanin FQ effect.
Zajac et al., Toulouse, France. In J Neurochem, Dec 2015
Moreover, siRNA knock-down of GRK2 indicated that GRK2, but not PKC, acted as the mediator in the NPFF anti-N/OFQ process.
Regulation of cellular oxidative stress and apoptosis by G protein-coupled receptor kinase-2; The role of NADPH oxidase 4.
Akhter et al., Chicago, United States. In Cell Signal, Dec 2015
We hypothesize that GRK2, a critical regulator of myocardial β-AR signaling, plays an important role in mediating cellular oxidative stress and apoptotic cell death in response to β-agonist stimulation.
Adrenal G protein-coupled receptor kinase-2 in regulation of sympathetic nervous system activity in heart failure.
Lymperopoulos et al., Fort Lauderdale, United States. In World J Cardiol, Oct 2015
Recent evidence indicates that adrenal GRK2 and βarrestins can regulate adrenal catecholamine secretion, thereby modulating SNS activity in HF.
G-protein-coupled receptor kinase 2 and endothelial dysfunction: molecular insights and pathophysiological mechanisms.
Kobayashi et al., Tokyo, Japan. In J Smooth Muscle Res, 2014
Recent studies have strongly implicated the involvement of G-protein-coupled receptor kinase 2 (GRK2) in the progression of cardiovascular disease.
[The Role of GRK2 and Its Potential as a New Therapeutic Target in Diabetic Vascular Complications].
Taguchi, In Yakugaku Zasshi, 2014
We identified G-protein-coupled receptor kinase 2 (GRK2) as a critical factor in diabetic endothelial dysfunction.
RKIP: a governor of intracellular signaling.
Deiss et al., Würzburg, Germany. In Crit Rev Oncog, 2013
In this work, we will review mechanistic details of the regulation of RKIP as inhibitor of Raf-1 and G protein-coupled receptor kinase 2 (GRK2) that enable RKIP to coordinate the cell's balance between inhibition and potentiation of mitogenic ERK1/2 signaling--a prominent example of RKIP's function as a regulator of intracellular signaling.
Elimination of GRK2 from cholinergic neurons reduces behavioral sensitivity to muscarinic receptor activation.
Caron et al., Durham, United States. In J Neurosci, 2012
This study demonstrated that the elimination of GRK2 in cholinergic neurons reduces sensitivity to select muscarinic-mediated behaviors
GRK2 contribution to the regulation of energy expenditure and brown fat function.
Fernández-Veledo et al., Madrid, Spain. In Faseb J, 2012
hemizygous mice displayed better thermogenic capacity and exhibited more oxidative phenotype in both BAT and WAT than WT littermates. Overexpression of GRK2 in brown adipocytes corroborated the negative effect in BAT function and differentiation
Raf kinase inhibitor protein (RKIP) dimer formation controls its target switch from Raf1 to G protein-coupled receptor kinase (GRK) 2.
Lorenz et al., Würzburg, Germany. In J Biol Chem, 2012
Data show that a dimeric Raf kinase inhibitor protein (RKIP) mutant displayed a higher affinity to G protein-coupled receptor kinase (GRK) 2, but a lower affinity to Raf1.
Inhibitor of G protein-coupled receptor kinase 2 normalizes vascular endothelial function in type 2 diabetic mice by improving β-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction.
Kobayashi et al., Tokyo, Japan. In Endocrinology, 2012
G protein-coupled receptor kinase 2 inhibitor normalizes vascular endothelial function in type 2 diabetic mice by improving beta-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction
Bidirectional regulation of neutrophil migration by mitogen-activated protein kinases.
Xu et al., Chicago, United States. In 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.
Roles of GRK2 in cell signaling beyond GPCR desensitization: GRK2-HDAC6 interaction modulates cell spreading and motility.
Mayor et al., Madrid, Spain. In Sci Signal, 2011
GRK2-HDAC6 functional interaction may have important implications in pathological contexts related to epithelial cell migration
GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood.
Cyster et al., San Francisco, United States. In Science, 2011
GRK2 functions in downregulation of S1PR1 on blood-exposed lymphocytes; GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate to lymphoid tissues
Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection.
Liew et al., Glasgow, United Kingdom. In Nat Med, 2010
Furthermore, we show that IL-33 reverses the TLR4-induced reduction of CXCR2 expression in neutrophils via the inhibition of expression of G protein-coupled receptor kinase-2 (GRK2), a serine-threonine protein kinase that induces internalization of chemokine receptors.
A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure.
Dorn et al., Cincinnati, United States. In Nat Med, 2008
Re-sequencing of GRK2 and GRK5 revealed a nonsynonymous polymorphism of GRK5, common in African Americans, in which leucine is substituted for glutamine at position 41.
Regulation of beta-adrenergic receptor signaling by S-nitrosylation of G-protein-coupled receptor kinase 2.
Stamler et al., Durham, United States. In Cell, 2007
findings show in tissues that S-nitrosothiols (SNOs) increase beta-adrenergic receptor (beta-AR) expression and prevent agonist-stimulated receptor downregulation; in cells, SNOs decrease GRK2-mediated beta-AR phosphorylation
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