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

G protein-coupled receptor 84

GPR84, GPCR4, EX33, G protein-coupled receptor 84
Top mentioned proteins: ACID, GPR120, GPR40, GPR43, CAN
Papers on GPR84
GPR84 and TREM-1 signaling contribute to the pathogenesis of reflux esophagitis.
Ulrich-Merzenich et al., Münster, Germany. In Mol Med, Dec 2015
The fatty acid receptor GPR84 was up-regulated in esophagitis but significantly decreased in treated groups, a finding supported by Western blot and immunohistochemistry in both rat tissue and HET-1A cells.
The role of G-protein receptor 84 in experimental neuropathic pain.
McMahon et al., London, United Kingdom. In J Neurosci, Jul 2015
G-protein receptor 84 (GPR84) is an orphan receptor that is induced markedly in monocytes/macrophages and microglia during inflammation, but its pathophysiological function is unknown.
GPR84 deficiency reduces microgliosis, but accelerates dendritic degeneration and cognitive decline in a mouse model of Alzheimer's disease.
Vallières et al., Québec, Canada. In Brain Behav Immun, May 2015
Under inflammatory conditions, these cells can express GPR84, an orphan receptor whose pathophysiological role is unknown.
Mutation analysis and molecular modeling for the investigation of ligand-binding modes of GPR84.
Takeda et al., Tokyo, Japan. In J Biochem, May 2015
GPR84 is a G protein-coupled receptor for medium-chain fatty acids.
Identification of Glial Activation Markers by Comparison of Transcriptome Changes between Astrocytes and Microglia following Innate Immune Stimulation.
Peterson et al., Hamilton, United States. In Plos One, 2014
In addition, other genes including Birc3 and Gpr84 as well as two expressed sequences AW112010 and BC023105 were found to be induced in both microglia and astrocytes and were upregulated in the CNS following virus infection.
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).
GeneChip expression profiling reveals the alterations of energy metabolism related genes in osteocytes under large gradient high magnetic fields.
Qian et al., Xi'an, China. In Plos One, 2014
12 energy metabolism related genes (PFKL, AK4, ALDOC, COX7A1, STC1, ADM, CA9, CA12, P4HA1, APLN, GPR35 and GPR84) were further confirmed by real-time PCR.
GPR84 sustains aberrant β-catenin signaling in leukemic stem cells for maintenance of MLL leukemogenesis.
Wang et al., Sydney, Australia. In Blood, 2014
Here we identified a novel β-catenin regulator, GPR84, a member of the G protein-coupled receptor family that represents a highly tractable class of drug targets.
Role of free fatty acid receptors in the regulation of energy metabolism.
Hirasawa et al., Kyoto, Japan. In Biochim Biophys Acta, 2014
However, only medium-chain FFAs, and not long-chain FFAs, activate GPR84 receptor.
A medium-chain fatty acid receptor Gpr84 in zebrafish: expression pattern and roles in immune regulation.
Liu et al., China. In Dev Comp Immunol, 2014
Gpr84 was recently identified as a receptor for medium-chain fatty acids, but its functions remain to be clarified.
Free fatty acids-sensing G protein-coupled receptors in drug targeting and therapeutics.
Hasegawa et al., Los Angeles, United States. In Curr Med Chem, 2012
In the past half decade, deorphanization of several GPCRs has revealed that GPR40, GPR41, GPR43, GPR84 and GPR120 sense concentration of extracellular FFAs with various carbon chain lengths.
Free fatty acid receptors and their role in regulation of energy metabolism.
Hirasawa et al., Kyoto, Japan. In Rev Physiol Biochem Pharmacol, 2012
FFARs are categorized according to the chain length of FFA ligands that activate each FFAR; FFA2 and FFA3 are activated by short chain FFAs, GPR84 is activated by medium-chain FFAs, whereas FFA1 and GPR120 are activated by medium- or long-chain FFAs.
Mining microarray datasets in nutrition: expression of the GPR120 (n-3 fatty acid receptor/sensor) gene is down-regulated in human adipocytes by macrophage secretions.
Denyer et al., Liverpool, United Kingdom. In J Nutr Sci, 2011
Exposure of the adipocytes to macrophage-conditioned medium for 4 or 24 h had no effect on GPR40 and GPR43 expression, but there was a marked stimulation of GPR84 expression (receptor for medium-chain fatty acids), the mRNA level increasing 13·5-fold at 24 h relative to unconditioned medium.
Targeting GPR120 and other fatty acid-sensing GPCRs ameliorates insulin resistance and inflammatory diseases.
Osborn et al., San Diego, United States. In Trends Pharmacol Sci, 2011
Free fatty acids (FFAs) have been demonstrated to act as ligands of several GPCRs including GPR40, GPR43, GPR84, GPR119 and GPR120.
The role of G-protein-coupled receptors in mediating the effect of fatty acids on inflammation and insulin sensitivity.
Lagakos et al., San Diego, United States. In Curr Opin Clin Nutr Metab Care, 2011
Deletion of GPR43 and GPR84 exacerbates inflammation, and deletion of the long-chain fatty acid receptors GPR119 and GPR120 reduces or is predicted to reduce glucose tolerance.
G protein-coupled receptor 84, a microglia-associated protein expressed in neuroinflammatory conditions.
Vallières et al., Québec, Canada. In Glia, 2007
in mice suffering from endotoxemia, microglia express GPR84 in a strong and sustained manner
The G-protein coupled receptor, GPR84 regulates IL-4 production by T lymphocytes in response to CD3 crosslinking.
Kuo et al., San Francisco, United States. In Immunol Lett, 2005
primary stimulation of T cells with anti-CD3 resulted in increased interleukin-4 but not interleukin-2 or interferon -gamma production in GPR84(-/-) mice compared to wild-type mice
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