P2RY5
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Purinergic receptor P2Y, G-protein coupled, 5
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Identifiers | ||||||||||||||
Symbol(s) | P2RY5; MGC120358; P2Y5 | |||||||||||||
External IDs | OMIM: 609239 MGI: 1914418 HomoloGene: 55925 | |||||||||||||
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RNA expression pattern | ||||||||||||||
Orthologs | ||||||||||||||
Human | Mouse | |||||||||||||
Entrez | 10161 | 67168 | ||||||||||||
Ensembl | ENSG00000139679 | ENSMUSG00000033446 | ||||||||||||
Uniprot | P43657 | Q8BMC0 | ||||||||||||
Refseq | NM_005767 (mRNA) NP_005758 (protein) |
NM_175116 (mRNA) NP_780325 (protein) |
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Location | Chr 13: 47.88 - 47.89 Mb | Chr 14: 71.97 - 71.97 Mb | ||||||||||||
Pubmed search | [1] | [2] |
Purinergic receptor P2Y, G-protein coupled, 5, also known as P2RY5, is a human gene.[1]
The protein encoded by this gene belongs to the family of G-protein coupled receptors, that are preferentially activated by adenosine and uridine nucleotides. This gene aligns with an internal intron of the retinoblastoma susceptibility gene in the reverse orientation.[1]
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[edit] Role In Hair Growth/Loss
In February 2008 researchers at the University of Bonn announced they have found the genetic basis of two distinct forms of inherited hair loss, opening a broad path to treatments for baldness. They found that the gene P2RY5 causes a rare, inherited form of hair loss called Hypotrichosis simplex. It is the first receptor in humans known to play a role in hair growth. The fact that any receptor plays a specific role in hair growth was previously unknown to scientists and with this new knowledge a focus on finding more of these genes may be able to lead to therapies for many different types of hair loss.[3][4]
[edit] See also
[edit] References
[edit] Further reading
- Ralevic V, Burnstock G (1998). "Receptors for purines and pyrimidines.". Pharmacol. Rev. 50 (3): 413-92. PMID 9755289.
- Toguchida J, McGee TL, Paterson JC, et al. (1993). "Complete genomic sequence of the human retinoblastoma susceptibility gene.". Genomics 17 (3): 535-43. doi: . PMID 7902321.
- Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides.". Gene 138 (1-2): 171-4. PMID 8125298.
- Herzog H, Darby K, Hort YJ, Shine J (1997). "Intron 17 of the human retinoblastoma susceptibility gene encodes an actively transcribed G protein-coupled receptor gene.". Genome Res. 6 (9): 858-61. PMID 8889552.
- Li Q, Schachter JB, Harden TK, Nicholas RA (1997). "The 6H1 orphan receptor, claimed to be the p2y5 receptor, does not mediate nucleotide-promoted second messenger responses.". Biochem. Biophys. Res. Commun. 236 (2): 455-60. doi: . PMID 9240460.
- Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, et al. (1997). "Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library.". Gene 200 (1-2): 149-56. PMID 9373149.
- Adrian K, Bernhard MK, Breitinger HG, Ogilvie A (2000). "Expression of purinergic receptors (ionotropic P2X1-7 and metabotropic P2Y1-11) during myeloid differentiation of HL60 cells.". Biochim. Biophys. Acta 1492 (1): 127-38. PMID 11004484.
- 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: . PMID 12477932.
- Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs.". Nat. Genet. 36 (1): 40-5. doi: . PMID 14702039.
- Dunham A, Matthews LH, Burton J, et al. (2004). "The DNA sequence and analysis of human chromosome 13.". Nature 428 (6982): 522-8. doi: . PMID 15057823.
- 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: . PMID 15489334.
- Ihara H, Hirukawa K, Goto S, Togari A (2005). "ATP-stimulated interleukin-6 synthesis through P2Y receptors on human osteoblasts.". Biochem. Biophys. Res. Commun. 326 (2): 329-34. doi: . PMID 15582581.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.