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Hydroxycarboxylic acid receptor 2

GPR109A, HM74A, PUMA-G, niacin receptor, HM74
putative G-protein coupled receptor for nicotinic acid [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, V1a, HDL, CAN, HAD
Papers on GPR109A
Central GPR109A Activation Mediates Glutamate-Dependent Pressor Response in Conscious Rats.
Abdel-Rahman et al., Carolina, Puerto Rico. In J Pharmacol Exp Ther, Feb 2016
G protein-coupled receptor 109A (GPR109A) activation by its ligand nicotinic acid (NA) in immune cells increases Ca(2+) levels, and Ca(2+) induces glutamate release and oxidative stress in central blood pressure (BP)-regulating nuclei, for example, the rostral ventrolateral medulla (RVLM), leading to sympathoexcitation.
Synthesis and Pharmacological Properties of Silicon-Containing GPR81 and GPR109A Agonists.
Tacke et al., Würzburg, Germany. In Chemmedchem, Dec 2015
The GPR81 and GPR109A receptors mediate antilipolytic effects and are potential drug targets for the treatment of metabolic disorders such as dyslipidemia and type 2 diabetes.
Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice.
Leung et al., Hong Kong, Hong Kong. In Nutrients, Sep 2015
In this regard, the role of the niacin receptor GPR109a in T2DM jejunal glucose transport remains unknown.
Low-dose niacin supplementation modulates GPR109A, niacin index and ameliorates Parkinson's disease symptoms without side effects.
Morgan et al., Augusta, United States. In Clin Case Rep, Jul 2015
A 65-year-old male, Parkinson's disease patient, was evaluated for GPR109A expression, niacin index, UPDRS scale, handwriting test, and quality of sleep with and without niacin treatment.
Dietary gut microbial metabolites, short-chain fatty acids, and host metabolic regulation.
Kimura et al., Fuchū, Japan. In Nutrients, Apr 2015
Short-chain fatty acids (SCFAs) such as acetate, butyrate, and propionate, which are produced by gut microbial fermentation of dietary fiber, are recognized as essential host energy sources and act as signal transduction molecules via G-protein coupled receptors (FFAR2, FFAR3, OLFR78, GPR109A) and as epigenetic regulators of gene expression by the inhibition of histone deacetylase (HDAC).
The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease.
Dixit et al., New Haven, United States. In Nat Med, Mar 2015
BHB blocks the NLRP3 inflammasome without undergoing oxidation in the TCA cycle, and independently of uncoupling protein-2 (UCP2), sirtuin-2 (SIRT2), the G protein-coupled receptor GPR109A or hydrocaboxylic acid receptor 2 (HCAR2).
A novel treatment target for Parkinson's disease.
Chong et al., Augusta, United States. In J Neurol Sci, 2015
GPR109A is a high-affinity niacin receptor.
M. tuberculosis Secretory Protein ESAT-6 Induces Metabolic Flux Perturbations to Drive Foamy Macrophage Differentiation.
Chatterjee et al., Farīdābād, India. In Sci Rep, 2014
Two major changes identified were the simultaneous buildup of DHAP (for Triglyceride synthesis) and AcCoA (for synthesis of 3-HB, ligand for the anti-lipolytic GPR109A).
GPR109A Expression in the Murine Min6 Pancreatic Beta Cell Line, and Its Relation with Glucose Metabolism and Inflammation.
Xu et al., Shantou, China. In Ann Clin Lab Sci, 2014
BACKGROUND: Nicotinic acid has been used clinically to manage dyslipidemia for many years, and its receptor, GPR109A, is expressed in various tissues or cells.
Nicotinic acid regulates glucose and lipid metabolism through lipid independent pathways.
Chen et al., Zibo, China. In Curr Pharm Biotechnol, 2014
NA exerts its anti-atherosclerotic or side effects via binding to GPR109A and receptor TRPV1.
Diet, metabolites, and "western-lifestyle" inflammatory diseases.
Mackay et al., Australia. In Immunity, 2014
Dietary-related metabolites engage "metabolite-sensing" G-protein-coupled receptors, such as GPR43, GPR41, GPR109A, GPR120, and GPR35.
Minireview: More than just a hammer: ligand "bias" and pharmaceutical discovery.
Luttrell, Charleston, United States. In Mol Endocrinol, 2014
Indeed, arrestin pathway-selective agonists for the type 1 parathyroid hormone and angiotensin AT1 receptors, and G protein pathway-selective agonists for the GPR109A nicotinic acid and μ-opioid receptors, have demonstrated unique, and potentially therapeutic, efficacy in cell-based assays and preclinical animal models.
Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis.
Ganapathy et al., Augusta, United States. In Immunity, 2014
GPR109A (encoded by Niacr1) is a receptor for butyrate in the colon.
GPR109a: the missing link between microbiome and good health?
Jobin, Gainesville, United States. In Immunity, 2014
In this issue of Immunity, Singh et al. (2014) demonstrate that microbial-derived butyrate mediated its protective activity against inflammation and colorectal cancer through GPR109a signaling.
International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands.
Harmar et al., Cambridge, United Kingdom. In Pharmacol Rev, 2013
The following recommendations are made for new receptor names based on 11 pairings for class A GPCRs: hydroxycarboxylic acid receptors [HCA₁ (GPR81) with lactate, HCA₂ (GPR109A) with 3-hydroxybutyric acid, HCA₃ (GPR109B) with 3-hydroxyoctanoic acid]; lysophosphatidic acid receptors [LPA₄ (GPR23), LPA₅ (GPR92), LPA₆ (P2Y5)]; free fatty acid receptors [FFA4 (GPR120) with omega-3 fatty acids]; chemerin receptor (CMKLR1; ChemR23) with chemerin; CXCR7 (CMKOR1) with chemokines CXCL12 (SDF-1) and CXCL11 (ITAC); succinate receptor (SUCNR1) with succinate; and oxoglutarate receptor [OXGR1 with 2-oxoglutarate].
Anti-inflammatory effects of nicotinic acid in human monocytes are mediated by GPR109A dependent mechanisms.
Choudhury et al., Oxford, United Kingdom. In Arterioscler Thromb Vasc Biol, 2012
Nicotnic acid displays a range of effects that are lipoprotein-independent and potentially antiatherogenic. These effects are mediated by GPR109A.
Distinct kinetic and spatial patterns of protein kinase C (PKC)- and epidermal growth factor receptor (EGFR)-dependent activation of extracellular signal-regulated kinases 1 and 2 by human nicotinic acid receptor GPR109A.
Zhou et al., Hangzhou, China. In J Biol Chem, 2011
upon binding to niacin GPR109A receptors initially activate G(i), leading to dissociation of the Gbetagamma subunit from activated G(i), and subsequently induce ERK1/2 activation via two distinct pathways.
Nicotinic acid inhibits glucose-stimulated insulin secretion via the G protein-coupled receptor PUMA-G in murine islet β cells.
Wei et al., Shantou, China. In Pancreas, 2011
Data show that high levels of PUMA-G transcripts and protein were detected in all beta cells.
Nicotinic acid receptor abnormalities in human skin cancer: implications for a role in epidermal differentiation.
Jacobson et al., Tucson, United States. In Plos One, 2010
In contrast, in a squamous cell carcinoma derived cell line, both GPR109A and GPR109B show a more diffuse cellular localization and the receptors are nearly non-functional.
High dietary niacin may increase prostaglandin formation but does not increase tumor formation in ApcMin/+ mice.
Lin et al., Torrance, United States. In Nutr Cancer, 2010
0.5-1% niacin in the daily diet activates the mouse GPR109A receptor.
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