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

G protein-coupled receptor kinase 1

rhodopsin kinase, G protein-coupled receptor kinase, GRK1
This gene encodes a member of the guanine nucleotide-binding protein (G protein)-coupled receptor kinase subfamily of the Ser/Thr protein kinase family. The protein phosphorylates rhodopsin and initiates its deactivation. Defects in GRK1 are known to cause Oguchi disease 2 (also known as stationary night blindness Oguchi type-2). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: GRK2, Rhodopsin, IRBP, CAN, ROD
Papers on rhodopsin kinase
GRK5 deficiency leads to susceptibility to intermittent hypoxia-induced cognitive impairment.
Suo et al., Kansas City, United States. In Behav Brain Res, Feb 2016
G protein-coupled receptor kinase-5 (GRK5) deficiency is recently found to render subjects more susceptible to cognitive impairment triggered by over-expression of Swedish mutant ß-amyloid precursor protein.
Conformational Selection in a Protein-Protein Interaction Revealed by Dynamic Pathway Analysis.
Kern et al., Oxford, United Kingdom. In Cell Rep, Feb 2016
Here, we present a direct demonstration of exclusive conformational selection in protein/protein recognition by measuring the flux for rhodopsin kinase binding to its regulator recoverin, an important molecular recognition in the vision system.
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.
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.
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
Heart failure (HF), the number one cause of death in the western world, is caused by the insufficient performance of the heart leading to tissue underperfusion in response to an injury or insult.
The retinal phenotype of Grk1-/- is compromised by a Crb1 rd8 mutation.
Craft et al., Los Angeles, United States. In Mol Vis, 2014
It was hypothesized that the G-protein receptor kinase 1 knockouts (Grk1(-/-) ), which were based on the B6N strain, would exhibit abnormal morphological phenotypes in their offspring not related to GRK1's major phosphorylation function.
Protein and Signaling Networks in Vertebrate Photoreceptor Cells.
Dell'Orco et al., Oldenburg, Germany. In Front Mol Neurosci, 2014
Illuminated rhodopsin is turned off by phosphorylation catalyzed by rhodopsin kinase (GRK1) under control of Ca(2+)-recoverin.
[Research on Molecular Mechanisms of Engulfment of Apoptotic Cells].
Nakaya, In Yakugaku Zasshi, 2014
We further determined that G protein-coupled receptor kinase 6 (GRK6), originally identified as a kinase responsible for the desensitization and downregulation of G-protein-coupled receptors, activates Rac1 independent of the two known intracellular engulfment pathways in phagocytes.
The importance of G protein-coupled receptor kinase 4 (GRK4) in pathogenesis of salt sensitivity, salt sensitive hypertension and response to antihypertensive treatment.
Ramesar et al., Cape Town, South Africa. In Int J Mol Sci, 2014
Salt sensitivity is probably caused by either a hereditary or acquired defect of salt excretion by the kidney, and it is reasonable to consider that this is the basis for differences in hypertension between black and white people.
Neuroinflammation and comorbidity of pain and depression.
Dantzer et al., Houston, United States. In Pharmacol Rev, 2013
These mechanisms include direct effects of cytokines on the neuronal environment or indirect effects via downregulation of G protein-coupled receptor kinase 2, activation of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase that generates neurotropic kynurenine metabolites, increased brain extracellular glutamate, and the switch of GABAergic neurotransmission from inhibition to excitation.
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.
A tale of two kinases in rods and cones.
Weiss et al., Chapel Hill, United States. In Adv Exp Med Biol, 2011
Defects in GRK1 or GRK7 cause patients to suffer from an inability to properly deactivate rhodopsin leading to problems with recovery and dark adaptation.
Oguchi disease masked by retinitis pigmentosa.
Miyake et al., Kumamoto, Japan. In Doc Ophthalmol, 2011
There are two genes that cause Oguchi disease: the G protein-coupled receptor kinase 1 gene and the S antigen gene. There is evidence that Oguchi disease and retinitis pigmentosa (RP) can coexist in the same family or even in the same individual
GIT1 is associated with ADHD in humans and ADHD-like behaviors in mice.
Kim et al., Taejŏn, South Korea. In Nat Med, 2011
Here we report a previously unidentified association between G protein-coupled receptor kinase-interacting protein-1 (GIT1) and ADHD in humans.
Nonenzymatic rapid control of GIRK channel function by a G protein-coupled receptor kinase.
Reuveny et al., Israel. In Cell, 2010
G protein-coupled receptors (GPCRs) respond to agonists to activate downstream enzymatic pathways or to gate ion channel function.
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 novel mutation in GRK1 causes Oguchi disease in a consanguineous Pakistani family.
Cremers et al., Islamabad, Pakistan. In Mol Vis, 2008
Genetic mapping supported the diagnosis of typical Oguchi disease in a Pakistani family and also resulted in the identification of a novel nonsense mutation (c.614C>A; p.S205X) in exon 1 of GRK1.
Amino acid residues in GRK1/GRK7 responsible for interaction with S-modulin/recoverin.
Kawamura et al., Ōsaka, Japan. In Photochem Photobiol, 2008
A GRK1 region close to its C-terminus also seemed to be the binding site for S-modulin/recoverin.
Novel mutations in the GRK1 gene in Japanese patients With Oguchi disease.
Yoshimura et al., Kyoto, Japan. In Am J Ophthalmol, 2007
The authors found two different novel mutations in Japanese patients. The results indicate that a considerable number of GRK1 mutations exist in the Japanese population.
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