gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

G protein-coupled receptor 132

This gene encodes a subfamily member of the G-protein couple receptor (GPCR) superfamily. The encoded protein is a high-affinity receptor for lysophosphatidylcholine (LPC), a major phospholipid component of oxidized low density lipoprotein. This protein may react to LPC levels at sites of inflammation to limit the expansion of tissue-infiltrating cells. A similar protein in mouse is involved in cell cycle progression. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CAN, V1a, GPR4, OGR1
Papers on G2A
Two zebrafish G2A homologs activate multiple intracellular signaling pathways in acidic environment.
Tomura et al., Kawasaki, Japan. In Biochem Biophys Res Commun, Feb 2016
Human G2A is activated by various stimuli such as lysophosphatidylcholine (LPC), 9-hydroxyoctadecadienoic acid (9-HODE), and protons.
Functional metagenomic discovery of bacterial effectors in the human microbiome and isolation of commendamide, a GPCR G2A/132 agonist.
Brady et al., New York City, United States. In Proc Natl Acad Sci U S A, Oct 2015
Commendamide resembles long-chain N-acyl-amides that function as mammalian signaling molecules through activation of G-protein-coupled receptors (GPCRs), which led us to the observation that commendamide activates the GPCR G2A/GPR132.
Activated microglia in ischemic stroke penumbra upregulate MCP-1 and CCR2 expression in response to lysophosphatidylcholine derived from adjacent neurons and astrocytes.
Shibata et al., Tokyo, Japan. In Neuropathology, Jun 2015
Furthermore, immunoreactivities for the LPC receptors G protein-coupled receptor 132 (G2A) and P2X purinoreceptor 7 (P2X7R), as well as the CC chemokine monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2, were detectable in activated microglia.
Acid sensitivity of the spinal dorsal root ganglia C-fiber nociceptors innervating the guinea pig esophagus.
Kollarik et al., Baltimore, United States. In Neurogastroenterol Motil, Jun 2015
Other evaluated targets (PKD2L1, TRPV4, TASK3, TALK1, G2A, GPR4, and TDAG8) were expressed rarely.
Oxidant/antioxidant status in children and adolescents with immune thrombocytopenia (ITP) and the role of an adjuvant antioxidant therapy.
Abdelaziz et al., Cairo, Egypt. In Pediatr Blood Cancer, May 2015
METHODS: Six months prospective randomized single blind study registered as (NCT 01763658) including 39 patients with newly diagnosed (ND) ITP; group 1 (G1) and 39 patients with chronic ITP (G2), each group was randomly allocated (2:1) to one of two subgroups respectively; (G1A and G2A) interventional arm received daily antioxidant therapy, while G1B and G2B; received a placebo.
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
In the cells that express proton-sensing GPCRs, including GPR4, OGR1, TDAG8, and G2A, extracellular acidification stimulates serum responsive element (SRE)-driven transcriptional activity, which has been shown to reflect Rho activity, with different proton sensitivities.
Nutritional factors (nutritional aspects) in biliary disorders: bile acid and lipid metabolism in gallstone diseases and pancreaticobiliary maljunction.
Kishikawa et al., Hiroshima, Japan. In J Gastroenterol Hepatol, 2013
Further, oxidized fatty acids have been established as a potent ligand for G2A, a member of G protein-coupled receptor family that mediates a diverse array of biological processes including cell growth and apoptosis.
Acidic tumor microenvironment and pH-sensing G protein-coupled receptors.
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.
Emerging roles for lysophosphatidylserine in resolution of inflammation.
Bratton et al., Denver, United States. In Prog Lipid Res, 2012
With regard to the latter, lysoPS generated in/on activated or aged apoptotic neutrophils enhances their clearance by macrophages via signaling through the macrophage G-protein coupled receptor G2A.
Therapeutic options for transfusion related acute lung injury; the potential of the G2A receptor.
Silliman et al., Denver, United States. In Curr Pharm Des, 2011
Lyso- PCs prime PMNs activating the G2A receptor and several inhibitors of this receptor, which could potentially be therapeutic in TRALI, have been identified.
Signaling via macrophage G2A enhances efferocytosis of dying neutrophils by augmentation of Rac activity.
Bratton et al., Denver, United States. In J Biol Chem, 2011
Lyso-PS signaled to macrophages in a G2A-dependent manner for their enhanced production of prostaglandin E2 (PGE2) via a calcium-dependent cytosolic phospholipase A2/cyclooxygenase-mediated mechanism.
HMGB1-directed drug discovery targeting cutaneous inflammatory dysregulation.
Wondrak et al., Tucson, United States. In Curr Drug Metab, 2010
Small molecule drugs that may provide therapeutic benefit through HMGB1-directed mechanisms involve HMGB1 inhibitory ligands, Toll-like receptor antagonists, RAGE antagonists, alpha7 nicotinic acetylcholine receptor agonists, G2A antagonists, serine protease inhibitors, and alpha-dicarbonyl-based soft electrophiles.
Identification and analysis of two splice variants of human G2A generated by alternative splicing.
Izumi et al., Maebashi, Japan. In J Pharmacol Exp Ther, 2010
we found an additional novel G2A variant (G2A-b) that is the major transcript with functional response to ligand stimulation as well as G2A-a, and succeeded in discriminating proton-sensing and oxidized fatty acid-sensing activities of G2A.
ApoE-dependent modulation of HDL and atherosclerosis by G2A in LDL receptor-deficient mice independent of bone marrow-derived cells.
Kabarowski et al., Birmingham, United States. In Arterioscler Thromb Vasc Biol, 2009
ApoE-dependent modulation of HDL and atherosclerosis by G2A in LDL receptor-deficient mice independent of bone marrow-derived cells.
Deletion of the G2A receptor fails to attenuate experimental autoimmune encephalomyelitis.
Kabarowski et al., Birmingham, United States. In J Neuroimmunol, 2009
study of the G2A-mediated effects in the pathophysiology of T cell-mediated autoimmune disease; it was concluded that the proposed anti-proliferative and chemotactic functions of G2A are not manifested in vivo
G2A deficiency in mice promotes macrophage activation and atherosclerosis.
Hedrick et al., Charlottesville, United States. In Circ Res, 2009
In the absence of G2A, increased macrophage activation and decreased apoptosis is associated with accumulation of macrophages in the aorta and increased atherosclerosis
Therapeutic effects of lysophosphatidylcholine in experimental sepsis.
Song et al., South Korea. In Nat Med, 2004
Incubation with an antibody to the LPC receptor, G2A, inhibited LPC-induced protection from CLP lethality and inhibited the effects of LPC in neutrophils.
Positron emission tomography imaging analysis of G2A as a negative modifier of lymphoid leukemogenesis initiated by the BCR-ABL oncogene.
Witte et al., Los Angeles, United States. In Cancer Cell, 2002
G2A is a negative modifier of lymphoid leukemogenesis initiated by the BCR-ABL oncogene
Lysophosphatidylcholine as a ligand for the immunoregulatory receptor G2A.
Xu et al., Cleveland, United States. In Science, 2001
We show that LPC is a high-affinity ligand for G2A, a lymphocyte-expressed G protein-coupled receptor whose genetic ablation results in the development of autoimmunity.
Mice lacking the orphan G protein-coupled receptor G2A develop a late-onset autoimmune syndrome.
Witte et al., Los Angeles, United States. In Immunity, 2001
Mice with a targeted disruption of the gene encoding a lymphoid-expressed orphan G protein-coupled receptor, G2A, demonstrate a normal pattern of T and B lineage differentiation through young adulthood.
share on facebooktweetadd +1mail to friends