The family of G-protein-coupled receptors includes many well-studied members, such as the adrenergic and the muscarinic acetylcholine receptors. These receptors are regulated by multiple mechanisms that serve to adapt their expression and their function to a rapidly changing environment. One of the most intriguing and important regulatory mechanisms involves the phosphorylation of such receptors by a set of specific kinases, termed the G-protein-coupled receptor kinases (GRKs). This phosphorylation is followed by binding of specific arrestin proteins to the phosphorylated receptors, which uncouples the receptors from their G proteins and thus causes a loss of receptor function. Several isoforms of the GRKs and the arrestins are expressed in the heart. They may be involved in the loss of receptor function in response to drugs. Furthermore, increased expression of one of the GRKs, β-adrenergic receptor kinase-1, has been found in failing hearts, and its increased activity may contribute to the loss of β
G-Protein-Coupled Receptor Kinases: A family of serine-threonine kinases that are specific for G-PROTEIN-COUPLED RECEPTORS. They are regulatory proteins that play a role in G-protein-coupled receptor densensitization.
Our data demonstrate the novel finding that GRK5 activity attenuates atherosclerosis, and that it does so through distinct antiatherogenic mechanisms in ECs, SMCs, monocytes, and Mϕs. These cell-specific mechanisms encompass diverse signaling systems, including the receptor tyrosine kinases CSF-1R and PDGFRβ, the 7-transmembrane receptor CCR2, the innate immunity receptors TLR4 and TNFR1, and the transcription factor NF-κB. Thus, despite data from overexpression and model cell systems suggesting the possibility that GRK5 could mediate proatherogenic activities,9,11,13,14 net physiological GRK5 activity clearly appears to be antiatherogenic.. Because GRK5-mediated phosphorylation of 7-transmembrane receptors promotes receptor/β-arrestin association,1 it may seem paradoxical that whereas GRK5 activity is antiatherogenic, β-arrestin2 activity is proatherogenic.19 However, at least 2 possibilities may help reconcile these findings. First, GRK5-mediated receptor phosphorylation may promote the ...
TY - JOUR. T1 - Agonist dose-dependent phosphorylation by protein kinase A and G protein-coupled receptor kinase regulates β2 adrenoceptor coupling to Gi proteins in cardiomyocytes. AU - Liu, Ruijie. AU - Ramani, Biswarathan. AU - Soto, Dagoberto. AU - De Arcangelis, Vania. AU - Xiang, Yang Kevin. PY - 2009/11/20. Y1 - 2009/11/20. N2 - Adrenoceptors receptors (ARs) play a pivotal role in regulating cardiovascular response to catecholamines during β2ARs, prototypical G protein-coupled receptors (GPCRs), expressed in animal hearts, display dual coupling to both Gs and Gi proteins to control the adenylyl cyclase-cAMP dependent protein kinase A (PKA) pathway to regulate contraction responses. Here, we showed that β2AR coupling to Gi proteins was agonist dose-dependent and occurred only at high concentrations in mouse cardiac myocytes. Both β2AR-induced PKA activity, measured by fluorescence resonance energy transfer (FRET) imaging, and the increase in myocyte contraction rate displayed ...
This study was initiated by revealing that two phases of dose-dependent Aβ effects existed in cultured microglial cells. One phase involves Aβ, in the micromolar range, directly inducing microglial TNF-α release as demonstrated previously (Meda et al., 1995). In addition to this known effect produced directly by Aβ, we discovered that, in the subthreshold nanomolar range, soluble Aβ, although insufficient to directly induce TNF-α release, can potentiate, in a dose-dependent manner, TNF-α release induced by other microglial activators, preferentially those that do so via GPCRs. Microglia-mediated inflammation is an important component of AD pathology (McGeer and McGeer, 2001). We showed recently that the ultimate coagulation factor, thrombin, a serine protease with elevated levels in AD brains (Akiyama et al., 1992), can activate microglial cells (as demonstrated by TNF-α induction, inducible nitric oxide synthase, and CD40 upregulation, etc.) via activation of G-protein-coupled PARs (Suo ...
The major finding of this study is that GIT1 is an important regulator of vascular remodeling. Specifically, we found that GIT1 depletion inhibited intima formation after carotid ligation by 50%. In vivo and in vitro analysis showed a key role for GIT1 in VSMC proliferation, migration, and apoptosis during vascular remodeling (Figure III in the online-only Data Supplement). Furthermore, GIT1 is required for VSMC proliferation through PLCγ and ERK1/2 by regulating the expression of cell cycle-related proteins, such as cyclin D1. GIT1 is also essential for cell survival by regulating VSMC apoptosis through PLCγ and cell migration through PLCγ and ERK1/2.. VSMC proliferation and migration are key components in vascular remodeling.1,2 The present study shows that GIT1 expression is highly regulated by AngII and PDGF in vitro, and during vascular remodeling in vivo. The role of GIT1 in mediating VSMC proliferation was demonstrated by several assays, including in vitro cell count, [3H]-thymidine ...
Background: Migration of leukocytes towards sites of inflammation, such as atherosclerotic lesions, is guided through chemokines, which interact with G protein-coupled receptors (GPCR) on leukocytes. This process is controlled by phosphorylation of these receptors through GPCR kinases (GRK). GRKs dampen the response of the chemokine signaling and as such regulate the migration of leukocytes towards the lesion. Given the major role of CCR1, CCR2, and CCR5 in atherogenesis, we focussed on GRK2 in this study, and assessed the role of GRK2 deficiency in haematopoietic cells on the atherogenic response in LDLr−/− mice.. Methods & Results: A bone marrow transplant was performed to generate LDLr−/− chimeras with a partial GRK2 deficiency in the haematopoietic lineage. GRK2+/− chimeras developed smaller lesions compared with wild-type controls (WT 585.0 ± 56.4x103 μm2 vs GRK2+/− 403.0 ± 43.8x103 μm2; p=0.017). Moreover, lesions in the GRK2+/− mice also had a 78% reduction in necrotic ...
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Complete information for GRK4 gene (Protein Coding), G Protein-Coupled Receptor Kinase 4, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Current projects emphasize attempts to understand regulation of the receptors and their desensitization which occurs in response to persistent stimulation. We are isolating the enzymes and proteins involved in these processes and studying their mechanisms of action in isolated protein and cellular systems as well as in whole animals. Most important are special enzymes called G protein-coupled receptor kinases which phosphorylate the receptors and lead to their desensitization which occurs when they bind a second protein called barrestin. Most recently we have been developing lines of transgenic animals in which these various proteins are either overexpressed or "knockedout" by homologous recombination. These genetically altered animal lines are helping to shed new light on the ways in which receptors are regulated. They also have suggested several novel approaches to human therapeutics ...
Current projects emphasize attempts to understand regulation of the receptors and their desensitization which occurs in response to persistent stimulation. We are isolating the enzymes and proteins involved in these processes and studying their mechanisms of action in isolated protein and cellular systems as well as in whole animals. Most important are special enzymes called G protein-coupled receptor kinases which phosphorylate the receptors and lead to their desensitization which occurs when they bind a second protein called barrestin. Most recently we have been developing lines of transgenic animals in which these various proteins are either overexpressed or "knockedout" by homologous recombination. These genetically altered animal lines are helping to shed new light on the ways in which receptors are regulated. They also have suggested several novel approaches to human therapeutics ...
G protein-coupled receptor kinase 2 promotes high-level Hedgehog signaling by regulating the active state of Smo through kinase-dependent and kinase-independent mechanisms in Drosophila ...
TY - JOUR. T1 - Paeoniflorin inhibits proliferation of fibroblast-like synoviocytes through suppressing G-protein-coupled receptor kinase 2. AU - Chen, Jing Yu. AU - Wu, Hua Xun. AU - Chen, Yin. AU - Zhang, Ling Ling. AU - Wang, Qingtong. AU - Sun, Wu Yi. AU - Wei, Wei. PY - 2012/3/13. Y1 - 2012/3/13. N2 - Paeoniflorin (Pae) is a monoterpene glucoside and the main component of the total glucosides of paeony (TGP) extracted from the roots of Paeonia lactiflora. Its anti-inflammatory effect is associated with regulating G-protein-coupled receptors (GPCRs) signaling. The aim of this study was to explore the expression change of G-protein-coupled receptor kinase 2 (GRK2) in fibroblast-like synoviocytes (FLS) and the effect of Pae. Pae was obtained and purified from the roots of Paeonia lactiflora. We investigated the expression of GRK2 in synovium during the inflammatory process and assessed the effects of a specific GRK2 inhibitor and Pae on proliferation, cAMP level, and protein kinase A (PKA) ...
Introduction]: Insulin resistance (IR) and obesity are major health problems and important risk factors for the development of non-alcoholic fatty liver disease, a disease spectrum that may include hepatic steatosis, non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. G protein-coupled receptor kinase 2 (GRK2), first identified as a regulator of G protein-coupled receptors (GPCRs), has been described to play a relevant role in the development of IR and obesity in vivo. However, the effect of GRK2 in the development of NASH had not been addressed so far. Since the deletion of GRK2 prevents excessive body weight gain, we fed WT and GRK2 global hemizygous mice (GRK2+/-) with a methionine and choline-deficient diet (MCD), a well stablished model of NASH that is independent of fat mass accretion. [Results]: Even though the MCD diet induced similar metabolic alterations and a comparable elevation in plasma transaminase activity in WT and GRK2+/- mice, other negative effects of the MCD were ...
The beta 2 adrenergic receptor (beta 2AR) undergoes desensitization by a process involving its phosphorylation by both protein kinase A (PKA) and G protein-coupled receptor kinases (GRKs). The protein kinase A-anchoring protein AKAP79 influences beta 2AR phosphorylation by complexing PKA with the receptor at the membrane. Here we show that AKAP79 also regulates the ability of GRK2 to phosphorylate agonist-occupied receptors. In human embryonic kidney 293 cells, overexpression of AKAP79 enhances agonist-induced phosphorylation of both the beta 2AR and a mutant of the receptor that cannot be phosphorylated by PKA (beta 2AR/PKA-). Mutants of AKAP79 that do not bind PKA or target to the beta 2AR markedly inhibit phosphorylation of beta 2AR/PKA-. We show that PKA directly phosphorylates GRK2 on serine 685. This modification increases Gbeta gamma subunit binding to GRK2 and thus enhances the ability of the kinase to translocate to the membrane and phosphorylate the receptor. Abrogation of the ...
The beta-adrenergic receptor kinase (beta ARK) phosphorylates the agonist-occupied beta-adrenergic receptor to promote rapid receptor uncoupling from Gs, thereby attenuating adenylyl cyclase activity. Beta ARK-mediated receptor desensitization may reflect a general molecular mechanism operative on many G-protein-coupled receptor systems and, particularly, synaptic neurotransmitter receptors. Two distinct cDNAs encoding beta ARK isozymes were isolated from rat brain and sequenced. The regional and cellular distributions of these two gene products, termed beta ARK1 and beta ARK2, were determined in brain by in situ hybridization and by immunohistochemistry at the light and electron microscopic levels. The beta ARK isozymes were found to be expressed primarily in neurons distributed throughout the CNS. Ultrastructurally, beta ARK1 and beta ARK2 immunoreactivities were present both in association with postsynaptic densities and, presynaptically, with axon terminals. The beta ARK isozymes have a ...
MGI protein superfamily detail pages represent the protein classification set for a homeomorphic superfamily from the Protein Information Resource SuperFamily (PIRSF) site.. Mouse superfamily members are shown with links to their corresponding HomoloGene Classes. Note that pseudogenes are included in PIRSF families but not in orthology sets used here. You can select a given mouse superfamily member and download (or forward to NCBI BLAST) FASTA formatted protein sequences of that mouse gene and its mouse, human and rat homologs, as defined in the corresponding HomoloGene Class. The numbers of mouse, human and rat genes in the HomoloGene Class are shown. You can also "Select all" mouse superfamily members to obtain their protein sequences and the protein sequences for all mouse, human and rat homologs of the mouse superfamily members.. The number of protein sequences returned does not always match the numbers of homologs shown, because the same protein sequence can be associated with multiple ...
SignaGen Laboratories, A Gene Delivery Company Providing Custom AAV Adenovirus Lentivirus Production Services & Manufacturing DNA/siRNA Transfection Reagents... Ad-GIT2 [SL100903] - Product Category: Human Adenovirus Type5 (dE1/E3) expressing G Protein-coupled Receptor Kinase Interactor 2 (GIT2) under a CMV promoter. Product Information Product Name: G Protein-coupled Receptor Kinase Interactor 2, pre-packaged adenovirus, ready to ship and ready to use format. Promoter: CMV Titer: 1E+10~1E+11 PFU/ml Storage Buffer: DMEM with 2.5% BSA, 2.5% glycerol Gene Information Gene Name: G
Title:Application of BRET for Studying G Protein-Coupled Receptors. VOLUME: 14 ISSUE: 5. Author(s):Agnieszka A. Kaczor, Magdalena Makarska-Bialokoz, Jana Selent, Rocio A. de la Fuente, Maria Marti-Solano and Marian Castro. Affiliation:Department of Synthesis and Chemical Technology of Pharmaceutical Substances with Computer Modeling Lab, Faculty of Pharmacy with Division of Medical Analytics, Medical University of Lublin, 4A Chodzki St., PL-20093 Lublin, Poland.. Keywords:BRET, G protein-coupled receptors, G protein-coupled receptor dimers.. Abstract:G protein-coupled receptors (GPCRs) constitute one of the largest classes of cell surface receptors. GPCR biology has been a subject of widespread interest owing to the functional relevance of these receptors and their potential importance in the development of new drugs. At present, over 30% of all launched drugs target these receptors. GPCRs have been considered for a long time to function as monomeric entities and the idea of GPCR dimerization ...
Increasing evidence suggests to vascular damage as an early contributor to the development of two leading causes of age-associated dementia, namely Alzheimer disease (AD) and AD-like pathology such as stroke. This review focuses on the role of G protein-coupled receptor kinases, particularly GRK2 as they relate to dementia and how the vascular abnormalities is involved in cerebrovascular pathogenesis. Any possible involvement of GRKs in AD pathogenesis is an interesting notion, whose exploration may help bridge the gap in our understanding of the heart-brain connection in relation to neurovisceral damage and vascular complications in AD. The a priori basis for this inquiry stems from the fact that kinases of this family regulate numerous receptor functions in the brain, the myocardium and elsewhere. The aim of this review is to discuss the finding of GRK2 overexpression in the context of the early AD pathogenesis, since increased levels of GRK2 immunoreactivity were found in vulnerable neurons from AD
GRK6 - GRK6 (untagged)-Kinase deficient mutant (K215M) of Human G protein-coupled receptor kinase 6 (GRK6), transcript variant 2 available for purchase from OriGene - Your Gene Company.
Next-day shipping cDNA ORF clones derived from GRK2 G protein-coupled receptor kinase 2 available at GenScript, starting from $99.00.
Activation of G protein-coupled receptors is involved in regulating many cellular responses, but less is known regarding the role of these receptors in the differentiation and maintenance of skeletal muscle. New findings implicate the inhibitor subunit Gαi2 as a vital mediator of myofiber maturation and growth, operating through multiple signaling pathways to selectively stimulate protein synthesis or inhibit cytokine-dependent protein turnover.. ...
Compare G Protein-coupled Receptor 113 ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
A ready-to-use reverse transfection format RNAi screening library targeting mouse GPCR genes. Just resuspend pre-dispensed siRNA, and add cells. Optimization plates available.
G protein-coupled receptors (GPCRs) comprise the largest family of cell surface signaling receptors in the mammalian genome, mediate cellular responses to diver...
pep:known chromosome:VEGA66:10:127747276:127751732:-1 gene:OTTMUSG00000027657 transcript:OTTMUST00000068436 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Gpr182 description:G protein-coupled receptor 182 ...
References for Abcams Recombinant human GRK7 protein (ab125599). Please let us know if you have used this product in your publication
Catalytic domain of the Protein Serine/Threonine Kinase, G protein-coupled Receptor Kinase 7. Serine/Threonine Kinases (STKs), G protein-coupled Receptor Kinase (GRK) subfamily, GRK7 isoform, catalytic (c) domain. STKs catalyze the transfer of the gamma-phosphoryl group from ATP to serine/threonine residues on protein substrates. The GRK subfamily is part of a larger superfamily that includes the catalytic domains of other protein STKs, protein tyrosine kinases, RIO kinases, aminoglycoside phosphotransferase, choline kinase, and phosphoinositide 3-kinase. GRKs phosphorylate and regulate G protein-coupled receptors (GPCRs), the largest superfamily of cell surface receptors, which regulate some part of nearly all physiological functions. Phosphorylated GPCRs bind to arrestins, which prevents further G protein signaling despite the presence of activating ligand. There are seven types of GRKs, named GRK1 to GRK7. GRK7, also called iodopsin kinase, belongs to the visual group of GRKs. It is primarily ...
A role of GRK2 in the regulation of blood pressure has been shown in animal models with partial germline deletion, universal GRK2 knockdown, and targeted overexpression or knockdown in vascular smooth muscle and endothelial cells.22, 33, 34, 35, 36 GRK2 plays an important role in the regulation of blood pressure.7 Germline deletion of Grk2 is lethal.37 GRK2 deficiency in global adult hemizygous mice (Grk2+/−) has no effect on basal blood pressure but increases the vasodilator response to acetylcholine or isoproterenol and protects against Ang II-induced hypertension and vascular remodeling that is partially caused by increased nitric oxide bioavailability.33 Cohn et al also found in mice that inhibition of vascular smooth muscle GRK2 by either overexpression of the C‐terminal portion of GRK2 or vascular smooth muscle-specific ablation of GRK2 protein expression has no effect on blood pressure.35 This method of GRK2 silencing also had no effect on the elevated blood pressure resulting from ...
387554453 - EP 1118621 A4 2003-06-25 - NOVEL G PROTEIN-COUPLED RECEPTOR PROTEIN AND DNA THEREOF - [origin: WO0020456A1] A human-origin G protein-coupled receptor protein or its peptide fragment or its salt, a nucleic acid encoding this receptor protein and its derivative, etc. The human hippocampus-origin G protein-coupled receptor protein or the nucleic acid encoding the same and its derivative are usable in determining a ligand (an agonist) to the G protein-coupled receptor protein, as preventives and/or remedies for diseases in association with dysfunction of the G protein-coupled receptor protein, as gene diagnostics, in a method for screening a compound capable of varying the expression dose of the G protein-coupled receptor protein or its peptide fragment, etc.[origin: WO0020456A1] A human-origin G protein-coupled receptor protein or its peptide fragment or its salt, a nucleic acid encoding this receptor protein and its derivative, etc. The human hippocampus-origin G protein-coupled receptor
Watterson, K., Johnston, E., Chalmers, C., Pronin, A., Cook, S., Benovic, J. and Palmer, T. (2002) Dual regulation of EDG1/S1P(1) receptor phosphorylation and internalization by protein kinase C and G-protein-coupled receptor kinase 2. Journal of Biological Chemistry, 277, pp. 5767-5777. (doi:10.1074/jbc.M110647200) ...
Figure 12. GPCR and heterotrimeric G-protein signalling.. The ligand bound to the GPCR is shown in red. Binding allows the exchange of GDP for GTP by the associated G protein, and dissociation of the protein into Gα and Gβγ subunits. These then have downstream effects on a range of proteins, thereby propagating the signal from the bound ligand. Yellow arrows indicate either activation (up arrow) or inhibition (down arrow) of the targets. Regulators of G-protein signalling (RGS) proteins aid the GTPase activity of the G protein to turn off the signal. Arrestin can bind the receptor following GPCR phosphorylation by G-protein receptor kinase (GRK), desensitizing the receptor to further signalling. Reproduced from Berridge, M.J. (2012) Cell Signalling Biology; doi:10.1042/csb0001002, with permission. ...
The G12 subfamily members Gα12 and Gα13 are well-documented as utilizing RhoGEFs as downstream signaling effectors. Crystallographic studies by Chen et al. [20] and Hajicek et al. [21] have provided intricate structural details of the interaction between Gα13 and the RH domain of p115RhoGEF, identifying a set of Gα13 residues that directly contact this target protein. The structure of Gα12 also has been elucidated, using a chimera comprised of amino acids 49-379 of Gα12 preceded by amino acids 1-28 of Gαi1[22]. However, a Gα12:RhoGEF complex has not been reported. In the current study, we utilized in vitro and cell-based approaches to examine the interaction between Gα12 and two putative target RhoGEFs, LARG and p115RhoGEF. Using immobilized RGS-homology (RH) domains of these RhoGEFs, we identified several substitutions of native amino acids in Gα12 that disrupted its binding to these proteins and blocked its ability to stimulate the Rho-dependent process of SRE-mediated transcription. ...
rat G protein-coupled receptor AGR9: a mammalian receptor, member of the G protein-coupled receptor family; expressed in cardiovascular, CNS & digestive systems; amino acid sequence given in first source
The large‐scale production of recombinant G protein-coupled receptors (GPCRs) is one of the major bottlenecks that hamper functional and structural studies of this important class of integral membrane proteins
Purchase G Protein-Coupled Receptors: Emerging Paradigms in Activation, Signaling and Regulation Part A, Volume 338 - 1st Edition. Print Book & E-Book. ISBN 9780128137727, 9780128137734
Dr. Koch would like to eventually perform large human trials to specifically look at levels of GRK2 to see if they can predict responses to drugs such as beta-blockers or other treatments for heart failure. We want to see in our proposed clinical trial if GRK2 can be a biomarker that can predict response to various therapies, he says. In animal models, we ve shown that when we lower GRK2 levels, the animal does better. We think that if a drug lowers GRK2 levels, the patient should benefit ...
G Protein‐Coupled Receptor Genetics: Research and Methods in the Post‐Genomic Era features practical techniques inspired by the fast moving GPCR field. From powerful bioinformatic tools tracing the e
By contrast, specific inhibition of endogenous GRK2 by dominant-negative mutants robustly inhibited OTR phosphorylation and internalization as well as arrestin/OTR interactions ...
Parmigiani RB, Magalhães GS, Galante PA, et al. (2005). "A novel human G protein-coupled receptor is over-expressed in prostate cancer". Genet. Mol. Res. 3 (4): 521-31. PMID 15688318 ...
Novel findings reveal that G protein-coupled receptors, which have previously assumed to be statically configured as monomers or dimers, can switch...
This gene encodes a member of the GIT protein family, which interact with G protein-coupled receptor kinases and possess ADP-ribosylation factor (ARF) GTPase-activating protein (GAP) activity. GIT proteins traffic between cytoplasmic complexes, focal adhesions, and the cell periphery, and interact with Pak interacting exchange factor beta (PIX) to form large oligomeric complexes that transiently recruit other proteins. GIT proteins regulate cytoskeletal dynamics and participate in receptor internalization and membrane trafficking. This gene has been shown to repress lamellipodial extension and focal adhesion turnover, and is thought to regulate cell motility. This gene undergoes extensive alternative splicing to generate multiple isoforms, but the full-length nature of some of these variants has not been determined. The various isoforms have functional differences, with respect to ARF GAP activity and to G protein-coupled receptor kinase 2 binding. [provided by RefSeq, Sep 2008 ...
There is considerable controversy over whether μ-opioid receptor (MOPr) desensitization is homologous or heterologous and over the mechanisms underlying such desensitization. In different cell types MOPr desensitization has been reported to involve receptor phosphorylation by various kinases, including G-protein-coupled receptor kinases (GRKs), second messenger and other kinases as well as perturbation of the MOPr effector pathway by GRK sequestration of G protein βγ subunits or ion channel modulation. Here we report that in brainstem locus coeruleus (LC) neurons prepared from relatively mature rats (5-8 weeks old) rapid MOPr desensitization induced by the high-efficacy opioid peptides methionine enkephalin and DAMGO was homologous and not heterologous to α2-adrenoceptors and somatostatin SST2 receptors. Given that these receptors all couple through G proteins to the same set of G-protein inwardly rectifying (GIRK) channels it is unlikely therefore that in mature neurons MOPr desensitization ...
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John Tesmer, a research associate professor at the Life Sciences Institute and the department of pharmacology at the University of Michigan Medical School, has been named the winner of the 2010 American Society for Biochemistry and Molecular Biology Young Investigator Award (formerly known as the ASBMB/Schering-Plough Research Institute Award), which honors outstanding research contributions to biochemistry and molecular biology by individuals who have no more than 15 years of postdoctoral experience.. Tesmer will present an award lecture titled "Structural Analysis of Heterotrimeric G Proteins and G Protein-Coupled Receptor Kinases" at 8:30 a.m. Monday, April 26, at the 2010 annual meeting in Anaheim, Calif.. G protein-coupled receptor signaling pathways are responsible for a wide range of intracellular events and are an intense area of biological and pharmaceutical study. Researchers studying GPCR owe a lot to Tesmer and his group, who provided insight into GPCR signaling through their ...
GIT2 - GIT2 (Myc-DDK-tagged)-Human G protein-coupled receptor kinase interacting ArfGAP 2 (GIT2), transcript variant 6 available for purchase from OriGene - Your Gene Company.