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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 3

one of several G-protein coupled receptors for the lysophospholipid ligand sphingosine 1-phosphate, activated adenylate cyclase [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: GPR12, GPCR, V1a, ACID, Phosphodiesterase
Papers on GPR3
Loss of GPR3 reduces the amyloid plaque burden and improves memory in Alzheimer's disease mouse models.
Thathiah et al., Leuven, Belgium. In Sci Transl Med, Nov 2015
The orphan G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptor (GPCR) GPR3 regulates activity of the γ-secretase complex in the absence of an effect on Notch proteolysis, providing a potential therapeutic target for Alzheimer's disease (AD).
Effects of aging on gene expression and mitochondrial DNA in the equine oocyte and follicle cells.
Carnevale et al., In Reprod Fertil Dev, Apr 2015
The aims of the study were to examine quantitative and temporal differences in mRNA for LH receptor (LHR), amphiregulin (AREG) and epiregulin (EREG) in granulosa cells, phosphodiesterase (PDE) 4D in cumulus cells and PDE3A, G-protein-coupled receptor 3 (GPR3), growth differentiation factor 9 (GDF9), bone morphogenetic protein 15 (BMP15) and mitochondrial (mt) DNA in oocytes.
Epigenetic dysregulation of hairy and enhancer of split 4 (HES4) is associated with striatal degeneration in postmortem Huntington brains.
Chen et al., Baltimore, United States. In Hum Mol Genet, Apr 2015
Neuron-specific mapping of the genome-wide distribution of H3K4me3 revealed 136 differentially enriched loci associated with genes implicated in neuronal development and neurodegeneration, including GPR3, TMEM106B, PDIA6 and the Notch signaling genes hairy and enhancer of split 4 (HES4) and JAGGED2, supporting the view that the neuronal epigenome is affected in HD.
CCL18 promotes epithelial-mesenchymal transition, invasion and migration of pancreatic cancer cells in pancreatic ductal adenocarcinoma.
Song et al., Shenyang, China. In Int J Oncol, Mar 2015
Intriguingly, pancreatic cancer cell lines expressed the potential CCL18 receptors PITPNM3, CCR6 and GPR3.
Mice lacking GPR3 receptors display late-onset obese phenotype due to impaired thermogenic function in brown adipose tissue.
George Kunos et al., Bethesda, United States. In Sci Rep, 2014
We report an unexpected link between aging, thermogenesis and weight gain via the orphan G protein-coupled receptor GPR3.
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).
The identification of GPR3 inverse agonist AF64394; the first small molecule inhibitor of GPR3 receptor function.
Watson et al., Copenhagen, Denmark. In Bioorg Med Chem Lett, 2014
The identification of the novel and selective GPR3 inverse agonist AF64394, the first small molecule inhibitor of GPR3 receptor function, is described.
β-arrestin 2 regulates Aβ generation and γ-secretase activity in Alzheimer's disease.
De Strooper et al., Leuven, Belgium. In Nat Med, 2013
Two GPCRs implicated previously in Alzheimer's disease (GPR3 and the β(2)-adrenergic receptor) mediate their effects on Aβ generation through interaction with β-arrestin 2. β-arrestin 2 physically associates with the Aph-1a subunit of the γ-secretase complex and redistributes the complex toward detergent-resistant membranes, increasing the catalytic activity of the complex.
Hormonal control of mammalian oocyte meiosis at diplotene stage.
Xia et al., Beijing, China. In Cell Mol Life Sci, 2012
This cAMP is generated through the activity of the Gs G-protein by the G-protein-coupled receptor, GPR3 and GPR12, and adenylyl cyclases (ADCY) endogenous to the oocyte.
GPR3 orphan receptor is involved in neuropathic pain after peripheral nerve injury and regulates morphine-induced antinociception.
Valverde et al., Barcelona, Spain. In Neuropharmacology, 2011
Involvement of the orphan GPR3 receptor is demonstrated for the first time in expression and development of neuropathic pain and in analgesia induced by morphine.
GPR3 may not be a potential candidate gene for premature ovarian failure.
Ma et al., Beijing, China. In Reprod Biomed Online, 2010
Mutations in GPR3 are not a common cause of premature ovarian failure in Chinese women.
The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons.
Merchiers et al., Leuven, Belgium. In Science, 2009
A high-throughput functional genomics screen identified G protein-coupled receptor 3 (GPR3), a constitutively active orphan G protein-coupled receptor, as a modulator of amyloid-beta production.
GPR3 receptor, a novel actor in the emotional-like responses.
Ledent et al., Barcelona, Spain. In Plos One, 2008
GPR3 qualifies as a new player in the modulation of behavioral responses to stress and constitutes a novel promising pharmacological target for treatment of emotional disorders
The Gs-linked receptor GPR3 inhibits the proliferation of cerebellar granule cells during postnatal development.
Saeki et al., Columbus, United States. In Plos One, 2008
GPR3 is a novel antiproliferative mediator of CGPs in the postnatal development of murine cerebellu
Generation of mouse oocytes defective in cAMP synthesis and degradation: endogenous cyclic AMP is essential for meiotic arrest.
Conti et al., Stanford, United States. In Dev Biol, 2008
Gpr3 is epistatic to Pde3a and fertility as well as meiotic arrest in the PDE3A-deficient oocyte is dependent on the activity of GPR3.
Genetic and phenotypic heterogeneity in ovarian failure: overview of selected candidate genes.
Simpson, Miami, United States. In Ann N Y Acad Sci, 2007
Genes that exert known hormonal effects (FSH, FSHR, LH, LHR, CYP17, CYP19) primarily affect follicle function, as do BMP15, GDF9, and GPR3.
[Oocyte-cumulus dialog].
Royère et al., Tours, France. In Gynecol Obstet Fertil, 2006
On the one hand, the oocyte will modulate follicle growth through specific gene expression (Figalpha, GDF-9, BMP15) as well as its meiosis (GPR3 et PDE3A).
Stops and starts in mammalian oocytes: recent advances in understanding the regulation of meiotic arrest and oocyte maturation.
Mehlmann, Farmington, United States. In Reproduction, 2005
This cAMP is generated by the oocyte, through the stimulation of the G(s) G-protein by the G-protein-coupled receptor, GPR3.
The Gs-linked receptor GPR3 maintains meiotic arrest in mammalian oocytes.
Jaffe et al., Farmington, United States. In Science, 2005
the GPR3 receptor is a link in communication between the somatic cells and oocyte of the ovarian follicle and is crucial for the regulation of meiosis
Vascular sphingosine-1-phosphate S1P1 and S1P3 receptors.
Salomone et al., United States. In Drug News Perspect, 2004
The sphingolipid sphingosine-1-phosphate (S1P) acts on five subtypes of G-protein- coupled receptors, termed S1P(1) (formerly endothelial differentiation gene-1 [Edg-1]), S1P(2) (Edg-5), S1P(3) (Edg-3), S1P(4) (Edg-6) and S1P(5) (Edg-8), and possibly several other "orphan" receptors, such as GPR3, GPR6 and GPR12.
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