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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Adrenergic, beta, receptor kinase 2

GRK3, beta-adrenergic receptor kinase 2, betaARK2
The beta-adrenergic receptor kinase specifically phosphorylates the agonist-occupied form of the beta-adrenergic and related G protein-coupled receptors. Overall, the beta adrenergic receptor kinase 2 has 85% amino acid similarity with beta adrenergic receptor kinase 1, with the protein kinase catalytic domain having 95% similarity. These data suggest the existence of a family of receptor kinases which may serve broadly to regulate receptor function. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: GRK2, GRK5, IRBP, GRK6, beta-arrestin
Papers on GRK3
β2- and β1-Adrenoceptor Expression Exhibits a Common Regulatory Pattern With GRK2 and GRK5 in Human and Animal Models of Cardiovascular Diseases.
New
DʼOcon et al., Valencia, Spain. In J Cardiovasc Pharmacol, Nov 2015
To explore if genic expression of β1- or β2-adrenoceptors (ARs) exhibits a common regulatory pattern with G protein-coupled receptor kinase (GRK) 2, GRK3, or GRK5 expression, we determined messenger RNA levels for these genes in different tissues from human and animal models of cardiovascular disease.
Mu opioid receptor stimulation activates c-Jun N-terminal kinase 2 by distinct arrestin-dependent and independent mechanisms.
New
Chavkin et al., Seattle, United States. In Cell Signal, Sep 2015
We compared JNK activation by morphine and fentanyl in JNK1(-/-), JNK2(-/-), JNK3(-/-), and GRK3(-/-) mice and found that both compounds specifically activate JNK2 in vivo; however, fentanyl activation of JNK2 was GRK3-dependent, whereas morphine activation of JNK2 was GRK3-independent.
Role of G Protein-Coupled Receptor Kinases 2 and 3 in μ-Opioid Receptor Desensitization and Internalization.
New
Bailey et al., Bristol, United Kingdom. In Mol Pharmacol, Aug 2015
In the present paper, we have used a novel membrane-permeable, small-molecule inhibitor of GRK2 and GRK3, Takeda compound 101 (Cmpd101; 3-[[[4-methyl-5-(4-pyridyl)-4H-1,2,4-triazole-3-yl] methyl] amino]-N-[2-(trifuoromethyl) benzyl] benzamidehydrochloride), to study the involvement of GRK2/3 in acute agonist-induced MOPr desensitization.
GRK3 suppresses L-DOPA-induced dyskinesia in the rat model of Parkinson's disease via its RGS homology domain.
Gurevich et al., Nashville, United States. In Sci Rep, 2014
Here we demonstrate that LID is attenuated by overexpression of GRK3 in the striatum, whereas knockdown of GRK3 by microRNA exacerbated it.
Loss of morphine reward and dependence in mice lacking G protein-coupled receptor kinase 5.
Schulz et al., Jena, Germany. In Biol Psychiatry, 2014
Using the hot-plate and conditioned place preference test, we investigated opioid-related antinociception and reward effects in mice lacking GRK3 or GRK5.
Evaluation of the role of g protein-coupled receptor kinase 3 in desensitization of mouse odorant receptors in a Mammalian cell line and in olfactory sensory neurons.
Touhara et al., Tokyo, Japan. In Chem Senses, 2014
Here we show that GRK3 attenuated the agonist responsiveness of a specific mouse odorant receptor for eugenol (mOR-EG) upon agonist pretreatment in HEK293 cells, but GRK3 did not affect the response amplitude or the recovery kinetics upon repeated agonist stimulation.
GRK3 is essential for metastatic cells and promotes prostate tumor progression.
Watnick et al., Houston, United States. In Proc Natl Acad Sci U S A, 2014
We discovered that G-protein-coupled receptor kinase 3 (GRK3; or β-adrenergic receptor kinase 2) was not only necessary for survival and proliferation of metastatic cells, but also sufficient to promote primary prostate tumor growth and metastasis upon exogenous expression in poorly metastatic cells in mouse xenograft models.
G protein-coupled receptor kinase-3-deficient mice exhibit WHIM syndrome features and attenuated inflammatory responses.
Siderovski et al., Chapel Hill, United States. In J Leukoc Biol, 2013
Recently, GRK3 was identified as a negative regulator of CXCL12/CXCR4 signaling that is defective in human WHIM syndrome.
Multiple functions of G protein-coupled receptor kinases.
Kurose et al., Fukuoka, Japan. In J Mol Signal, 2013
In contrast, GRK2, GRK3, GRK5, and GRK6 are ubiquitously expressed throughout the body.
Functions of third extracellular loop and helix 8 of Family B GPCRs complexed with RAMPs and characteristics of their receptor trafficking.
Review
Kato et al., Miyazaki, Japan. In Curr Protein Pept Sci, 2013
In addition, we demonstrated that overexpression of GPCR kinase (GRK) 2, GRK3 and GRK4 enhances the AM-induced internalization of the CLR/RAMP2 heterodimer.
Serine 129 phosphorylation of membrane-associated α-synuclein modulates dopamine transporter function in a G protein-coupled receptor kinase-dependent manner.
Kato et al., Yamagata, Japan. In Mol Biol Cell, 2013
Subcellular fractionation of small interfering RNA (siRNA)-treated cells shows that G protein-coupled receptor kinase 3 (GRK3), GRK5, GRK6, and casein kinase 2 (CK2) contribute to Ser-129 phosphorylation of membrane-associated α-syn, whereas cytosolic α-syn is phosphorylated exclusively by CK2.
Activity of β2-adrenergic receptor in oral squamous cell carcinoma is mediated by overexpression of the ADRBK2 gene: a pilot study.
GeneRIF
García-García et al., Santiago de Compostela, Spain. In Biotech Histochem, 2012
In oral squamous cell carcinomas, malignant cells and surrounding tissue overexpress the ADRBK2 gene.
Molecular and cell signaling targets for PTSD pathophysiology and pharmacotherapy.
Review
Oakley et al., San Diego, United States. In Neuropharmacology, 2012
GRK3 phosphorylation of the CRF(1) receptor protein and subsequent binding of βarrestin2 rapidly terminate Gs-coupled CRF(1) receptor signaling by homologous desensitization.
Suppression of G-protein-coupled receptor kinase 3 expression is a feature of classical GBM that is required for maximal growth.
GeneRIF
Rubin et al., Saint Louis, United States. In Mol Cancer Res, 2012
GRK3 is a negative regulator of cell growth whose expression is preferentially reduced in glioblastoma of the classical subtype as a consequence of activity in primary gliomagenic pathways.
Reduced expression of G protein-coupled receptor kinases in schizophrenia but not in schizoaffective disorder.
GeneRIF
Gurevich et al., Nashville, United States. In Neurobiol Dis, 2011
A reduced cortical concentration of GRK3 in schizophrenia (resembling that in aging) may result in altered G protein-dependent signaling, thus contributing to prefrontal deficits in schizophrenia.
Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: a potential link to stress resilience.
GeneRIF
Eikenburg et al., Houston, United States. In Behav Brain Res, 2011
We suggest that reduced stress resilience after TSS may be related to oxidative stress, depletion of GRK3 and impaired regulation of alpha(2A)-AR and CRF(1)-R in LC.
beta-Adrenoceptor and GRK3 expression in human lymphocytes is related to blood pressure and urinary albumin excretion.
GeneRIF
D'Ocon et al., Valencia, Spain. In J Hypertens, 2010
mRNA levels for GRK3 were inversely correlated with systolic and diastolic blood pressure (day, night and 24 h), which suggests a protective role for GRK3 in the regulation of human blood pressure
The involvement of GSK3beta in bipolar disorder: integrating evidence from multiple types of genetic studies.
Review
Ophoff et al., Utrecht, Netherlands. In Eur Neuropsychopharmacol, 2010
The genes most consistently associated with BD in the genetic studies we reviewed were GSK3beta , GRK3, 5-HTTLPR, GRIN3, COMT, and GLUR3.
Genetics of bipolar disorder.
Review
Kato et al., Wako, Japan. In Drugs Today (barc), 2005
Among recently reported candidate genes, BDNF, G72, AKT1, GRIN2A, XBP1, GRK3, HTR4, IMPA2 and GABRA1 may have some importance.
Non-visual GRKs: are we seeing the whole picture?
Review
Nahorski et al., Leicester, United Kingdom. In Trends Pharmacol Sci, 2003
Studies of the details and consequences of these mechanisms have focused heavily on the original beta-adrenoceptor kinase (beta-ARK) family (GRK2 and GRK3) and, in particular, on phosphorylation-dependent recruitment of adaptor proteins such as the beta-arrestins.
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