GPR119
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GPR119, G protein-spregnuti receptor 119, je protein koji je kod čoveka kodiran GPR119 genom.[1]
G protein-spregnuti receptor 119 | |||||||||||
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Identifikatori | |||||||||||
Simboli | GPR119; GPCR2; MGC119957; hGPCR2 | ||||||||||
Vanjski ID | OMIM: 300513 MGI: 2668412 HomoloGene: 18670 IUPHAR: GPR119 GeneCards: GPR119 Gene | ||||||||||
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Pregled RNK izražavanja | |||||||||||
podaci | |||||||||||
Ortolozi | |||||||||||
Vrsta | Čovek | Miš | |||||||||
Entrez | 139760 | 236781 | |||||||||
Ensembl | ENSG00000147262 | ENSMUSG00000051209 | |||||||||
UniProt | Q8TDV5 | Q2ABS2 | |||||||||
RefSeq (mRNA) | NM_178471 | NM_181751 | |||||||||
RefSeq (protein) | NP_848566 | NP_861416 | |||||||||
Lokacija (UCSC) | Chr X: 129.35 - 129.35 Mb | Chr X: 44.92 - 44.92 Mb | |||||||||
PubMed pretraga | [1] | [2] |
GPR119, zajedno sa GPR55 i GPR18, se smatra da su kanabinoidni receptori.[2][3][4]
Farmakologija
urediGPR119 je izražen predominantno u pankreasu i gastrointestinalnom traktu kod glodara i čoveka, kao i u mozgu glodara.[5] Za aktivaciju receptora je bilo pokazano da uzrokuje redukciju unosa hrane i povećanja telesne težine kod pacova.[5] Za GPR119 je takođe bilo pokazano da reguliše izlučivanje hormona inkretina i insulina.[6][7][8] Iz tih razloga je bilo predloženo da novi lekovi koji bi delovali na ovaj receptor možda mogu da budu korisni u lečenju gojaznosti i dijabetesa.[5][9][10]
Ligandi
urediViše endogenih i sintetičkih liganda ovog receptora je bilo identifikovano:[11][12][13]
Reference
uredi- ↑ „Entrez Gene: GPR119 G protein-coupled receptor 119”.
- ↑ Brown AJ (November 2007). „Novel cannabinoid receptors”. Br. J. Pharmacol. 152 (5): 567–75. DOI:10.1038/sj.bjp.0707481. PMC 2190013. PMID 17906678.
- ↑ Izzo AA, Sharkey KA (April 2010). „Cannabinoids and the gut: new developments and emerging concepts”. Pharmacology & Therapeutics 126 (1): 21–38. DOI:10.1016/j.pharmthera.2009.12.005. PMID 20117132.
- ↑ McHugh D, Hu SS, Rimmerman N, Juknat A, Vogil Z, Walker JM, Bradshaw HB (March 2010). „N-arachidonoyl glycine, an abundant endogenous lipid, potently drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor”. BMC Neuroscience 11 (1): 44. DOI:10.1186/1471-2202-11-44. PMC 2865488. PMID 20346144.
- ↑ 5,0 5,1 5,2 5,3 5,4 5,5 Overton HA, Babbs AJ, Doel SM, Fyfe MC, Gardner LS, Griffin G, Jackson HC, Procter MJ, Rasamison CM, Tang-Christensen M, Widdowson PS, Williams GM, Reynet C. (2006). „Deorphanization of a G protein-coupled receptor for oleoylethanolamide and its use in the discovery of small-molecule hypophagic agents.”. Cell Metab. 3 (3): 167–175. DOI:10.1016/j.cmet.2006.02.004. PMID 16517404.
- ↑ 6,0 6,1 Ning Y, O'Neill K, Lan H, Pang L, Shan LX, Hawes BE, Hedrick JA. (2008). „Endogenous and synthetic agonists of GPR119 differ in signalling pathways and their effects on insulin secretion in MIN6c4 insulinoma cells.”. Br J Pharmacol. 155 (7): 1056–65. DOI:10.1038/bjp.2008.337. PMC 2528830. PMID 18724386.
- ↑ Swaminath G. (2008). „Fatty acid binding receptors and their physiological role in type 2 diabetes.”. Arch Pharm (Weinheim). 341 (12): 753–761. DOI:10.1002/ardp.200800096. PMID 19009545.
- ↑ Lan H, Vassileva G, Corona A, Liu L, Baker H, Golovko A, Abbondanzo SJ, Hu W, Yang S, Ning Y, Del Vecchio RA, Poulet F, Laverty M, Gustafson EL, Hedrick JA, Kowalski TJ. (2009). „GPR119 is required for physiological regulation of glucagon-like peptide-1 secretion but not for metabolic homeostasis.”. J Endocrinol. 201 (2): 219–230. DOI:10.1677/JOE-08-0453. PMID 19282326.
- ↑ Swaminath G. (2008). „Fatty acid binding receptors and their physiological role in type 2 diabetes.”. Arch Pharm (Weinheim). 341 (12): 753–761. DOI:10.1002/ardp.200800096. PMID 19009545.
- ↑ 10,0 10,1 10,2 Overton HA, Fyfe MC, Reynet C. (2007). „GPR119, a novel G protein-coupled receptor target for the treatment of type 2 diabetes and obesity.”. Br J Pharmacol. 153 (Suppl 1): S76–81. DOI:10.1038/sj.bjp.0707529. PMC 2268073. PMID 18037923.
- ↑ Shah U (July 2009). „GPR119 agonists: a promising new approach for the treatment of type 2 diabetes and related metabolic disorders”. Current Opinion in Drug Discovery & Development 12 (4): 519–32. PMID 19562648.
- ↑ Godlewski G, Offertáler L, Wagner JA, Kunos G (September 2009). „Receptors for acylethanolamides-GPR55 and GPR119”. Prostaglandins & Other Lipid Mediators 89 (3-4): 105–11. DOI:10.1016/j.prostaglandins.2009.07.001. PMC 2751869. PMID 19615459.
- ↑ Wu Y, Kuntz JD, Carpenter AJ, Fang J, Sauls HR, Gomez DJ, Ammala C, Xu Y, Hart S, Tadepalli S (April 2010). „2,5-Disubstituted pyridines as potent GPR119 agonists”. Bioorganic & Medicinal Chemistry Letters 20 (8): 2577–81. DOI:10.1016/j.bmcl.2010.02.083. PMID 20227877.
- ↑ Semple G, Fioravanti B, Pereira G, Calderon I, Uy J, Choi K, Xiong Y, Ren A, Morgan M, Dave V, Thomsen W, Unett DJ, Xing C, Bossie S, Carroll C, Chu ZL, Grottick AJ, Hauser EK, Leonard J, Jones RM. (2008). „Discovery of the first potent and orally efficacious agonist of the orphan G-protein coupled receptor 119.”. J Med Chem. 51 (17): 5172–5175. DOI:10.1021/jm8006867. PMID 18698756.
- ↑ Jones RM, Leonard JN, Buzard DJ, Lehmann J (October 2009). „GPR119 agonists for the treatment of type 2 diabetes”. Expert Opin Ther Pat 19 (10): 1339–59. DOI:10.1517/13543770903153878. PMID 19780700.
- ↑ Brown AJ. (2007). „Novel cannabinoid receptors.”. Br J Pharmacol. 152 (5): 567–575. DOI:10.1038/sj.bjp.0707481. PMC 2190013. PMID 17906678.
- ↑ Ning Y, O'Neill K, Lan H, Pang L, Shan LX, Hawes BE, Hedrick JA. (2008). „Endogenous and synthetic agonists of GPR119 differ in signaling pathways and their effects on insulin secretion in MIN6c4 insulinoma cells.”. Br J Pharmacol. 155 (7): 1056–65. DOI:10.1038/bjp.2008.337. PMC 2528830. PMID 18724386.
- ↑ Godlewski G, Offertáler L, Wagner JA, Kunos G (September 2009). „Receptors for acylethanolamides-GPR55 and GPR119”. Prostaglandins & Other Lipid Mediators 89 (3-4): 105–11. DOI:10.1016/j.prostaglandins.2009.07.001. PMC 2751869. PMID 19615459. Pristupljeno 2011-04-09.
Literatura
uredi- Takeda S, Kadowaki S, Haga T, et al. (2002). „Identification of G protein-coupled receptor genes from the human genome sequence.”. FEBS Lett. 520 (1-3): 97–101. DOI:10.1016/S0014-5793(02)02775-8. PMID 12044878.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). „Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.”. Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. DOI:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Fredriksson R, Höglund PJ, Gloriam DE, et al. (2003). „Seven evolutionarily conserved human rhodopsin G protein-coupled receptors lacking close relatives.”. FEBS Lett. 554 (3): 381–8. DOI:10.1016/S0014-5793(03)01196-7. PMID 14623098.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). „The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).”. Genome Res. 14 (10B): 2121–7. DOI:10.1101/gr.2596504. PMC 528928. PMID 15489334.
- Ross MT, Grafham DV, Coffey AJ, et al. (2005). „The DNA sequence of the human X chromosome.”. Nature 434 (7031): 325–37. DOI:10.1038/nature03440. PMC 2665286. PMID 15772651.
- Overton HA, Babbs AJ, Doel SM, et al. (2006). „Deorphanization of a G protein-coupled receptor for oleoylethanolamide and its use in the discovery of small-molecule hypophagic agents.”. Cell Metab. 3 (3): 167–75. DOI:10.1016/j.cmet.2006.02.004. PMID 16517404.