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

G protein-coupled receptor 4

GPR4, GPR19, G protein-coupled receptor 4
orphan G-protein coupled receptor, similar to D2 dopamine and adrenergic receptors [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: OGR1, ACID, G2A, TDAG8, V1a
Papers on GPR4
Proton detection and breathing regulation by the retrotrapezoid nucleus.
New
Wenker et al., Basel, Switzerland. In J Physiol, Feb 2016
In vitro, their activation by [H(+) ] requires expression of a proton-activated GPCR (GPR4) and a proton-modulated potassium channel (TASK-2) whose transcripts are undetectable in astrocytes and the rest of the lower brainstem respiratory network.
Adropin Acts in Brain to Inhibit Water Drinking: Potential Interaction with the Orphan G Protein-Coupled Receptor, GPR19.
New
Samson et al., Saint-Louis, Senegal. In Am J Physiol Regul Integr Comp Physiol, Feb 2016
We describe a central nervous system action of adropin to inhibit water drinking and identify a potential adropin receptor, the orphan G protein-coupled receptor, GPR19.
Lgr4 controls specialization of female gonads in mice.
New
Nishimori et al., Japan. In Biol Reprod, Oct 2015
Leucine-rich repeat-containing G protein-coupled receptor 4 (Lgr4) is a type of membrane receptor with a seven-transmembrane structure.
Neural Control of Breathing and CO2 Homeostasis.
Review
New
Bayliss et al., Charlottesville, United States. In Neuron, Oct 2015
RTN neurons detect CO2 via intrinsic proton receptors (TASK-2, GPR4), synaptic input from peripheral chemoreceptors and signals from astrocytes.
Ablation of Lgr4 enhances energy adaptation in skeletal muscle via activation of Ampk/Sirt1/Pgc1α pathway.
New
Ning et al., Shanghai, China. In Biochem Biophys Res Commun, Sep 2015
Leucine-rich repeat-containing G protein-coupled receptor 4 (Lgr4) is a newfound obese-associated gene.
Increased expression of the proton-sensing G protein-coupled receptor Gpr65 during retinal degeneration.
New
Grimm et al., Zürich, Switzerland. In Neuroscience, Sep 2015
GPR4, GPR65 and GPR68 are G protein-coupled receptors that aid cells to sense and survive conditions of acidic pH and inflammatory cells express Gpr65 enhancing their viability.
Adaptation by the collecting duct to an exogenous acid load is blunted by deletion of the proton-sensing receptor GPR4.
New
Petrovic et al., Winston-Salem, United States. In Am J Physiol Renal Physiol, Aug 2015
We previously reported that the deletion of the pH sensor GPR4 causes a non-gap metabolic acidosis and defective net acid excretion (NAE) in the GPR4 knockout mouse (GPR4-/-) (Sun X, Yang LV, Tiegs BC, Arend LJ, McGraw DW, Penn RB, and Petrovic S. J Am Soc Nephrol 21: 1745-1755, 2010).
PHYSIOLOGY. Regulation of breathing by CO₂ requires the proton-activated receptor GPR4 in retrotrapezoid nucleus neurons.
New
Impact
Bayliss et al., Charlottesville, United States. In Science, Jul 2015
We show that selective expression of the proton-activated receptor GPR4 in chemosensory neurons of the mouse retrotrapezoid nucleus (RTN) is required for CO2-stimulated breathing.
Characterization of Imidazopyridine Compounds as Negative Allosteric Modulators of Proton-Sensing GPR4 in Extracellular Acidification-Induced Responses.
Okajima et al., Maebashi, Japan. In Plos One, 2014
G protein-coupled receptor 4 (GPR4), previously proposed as the receptor for sphingosylphosphorylcholine, has recently been identified as the proton-sensing G protein-coupled receptor (GPCR) coupling to multiple intracellular signaling pathways, including the Gs protein/cAMP and G13 protein/Rho.
Constitutive Activity among Orphan Class-A G Protein Coupled Receptors.
Aronstam et al., Rolla, United States. In Plos One, 2014
Five patterns of activity were noted: 1) inhibition under both baseline and forskolin stimulated expression (GPR15, GPR17, GPR18, GPR20, GPR25, GPR27, GPR31, GPR32, GPR45, GPR57, GPR68, GPR83, GPR84, GPR132, GPR150, GPR176); 2) no effect on baseline expression, but inhibition of forskolin stimulated expression (GPR4, GPR26, GPR61, GPR62, GPR78, GPR101, GPR119); 3) elevation of baseline signaling coupled with inhibition of forskolin stimulated expression (GPR6, GPR12); 4) elevation of baseline signaling without inhibition of forskolin stimulated expression (GPR3, GPR21, GPR52, GPR65); and 5) no effect on expression (GPR1, GPR19, GPR22, GPR34, GPR35, GPR39, GPR63, GPR82, GPR85, GPR87).
pH sensing and regulation in cancer.
Review
Gillies et al., Tampa, United States. In Front Physiol, 2012
However, there is evidence that expression of proton-sensing GPCRs such as GPR4, TDAG8, and OGR1 can regulate aspects of tumorigenesis and invasion, including cofilin and talin regulated actin (de-)polymerization.
Acidic tumor microenvironment and pH-sensing G protein-coupled receptors.
Review
Yang et al., Greenville, United States. In Front Physiol, 2012
Recent studies show that the pH-sensing GPCRs, including GPR4, GPR65 (TDAG8), GPR68 (OGR1), and GPR132 (G2A), regulate cancer cell metastasis and proliferation, immune cell function, inflammation, and blood vessel formation.
Molecular mechanisms of acid-base sensing by the kidney.
Review
Wagner et al., Boston, United States. In J Am Soc Nephrol, 2012
Over the past few years, however, some candidate molecular pH sensors have been identified, including acid/alkali-sensing receptors (GPR4, InsR-RR), kinases (Pyk2, ErbB1/2), pH-sensitive ion channels (ASICs, TASK, ROMK), and the bicarbonate-stimulated adenylyl cyclase (sAC).
Inhibition of tumor cell migration and metastasis by the proton-sensing GPR4 receptor.
GeneRIF
Yang et al., Greenville, United States. In Cancer Lett, 2012
findings suggest that GPR4 activation by an acidic pH inhibits tumor cell migration and invasion, and the Rho GTPase is at least partly responsible for this phenotype
Reduced pathological angiogenesis and tumor growth in mice lacking GPR4, a proton sensing receptor.
GeneRIF
Ludwig et al., Basel, Switzerland. In Angiogenesis, 2011
Reduced pathological angiogenesis and tumor growth in mice lacking GPR4, a proton sensing receptor.
Activation of GPR4 by acidosis increases endothelial cell adhesion through the cAMP/Epac pathway.
GeneRIF
Yang et al., Greenville, United States. In Plos One, 2010
acidosis/GPR4 signaling regulates endothelial cell adhesion mainly through the G(s)/cAMP/Epac pathway
Deletion of the pH sensor GPR4 decreases renal acid excretion.
GeneRIF
Petrovic et al., Cincinnati, United States. In J Am Soc Nephrol, 2010
pH sensor with an important role in regulating acid secretion in the kidney collecting duct
Each one of certain histidine residues in G-protein-coupled receptor GPR4 is critical for extracellular proton-induced stimulation of multiple G-protein-signaling pathways.
GeneRIF
Okajima et al., Maebashi, Japan. In Pharmacol Res, 2010
The mutation of histidine residue at 79, 165, or 269 from the N-terminal of GPR4 to phenylalanine shifted the half-maximal effective concentration (EC(50)) of proton-induced signaling activities to the right, including cAMP accumulation.
Receptors for protons or lipid messengers or both?
Review
Wolf et al., Basel, Switzerland. In J Recept Signal Transduct Res, 2005
The subfamily of G protein-coupled receptors comprising GPR4, OGR1, TDAG8, and G2A was originally characterized as a group of proteins mediating biological responses to the lipid messengers sphingosylphosphorylcholine (SPC), lysophosphatidylcholine (LPC), and psychosine.
Proton-sensing G-protein-coupled receptors.
Impact
GeneRIF
Seuwen et al., Basel, Switzerland. In Nature, 2003
GPR4, a close relative of OGR1, also responds to pH changes, but elicits cyclic AMP formation
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