Jump to content

Prokineticin receptor 2

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Boghog (talk | contribs) at 04:44, 23 August 2016 (removed no longer needed PBB controls and templates; consistent citation formatting; removed further reading citations not specific to this gene). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

PROKR2
Identifiers
AliasesPROKR2, GPR73L1, GPR73b, GPRg2, HH3, KAL3, PKR2, dJ680N4.3, prokineticin receptor 2
External IDsOMIM: 607123; MGI: 2181363; HomoloGene: 16368; GeneCards: PROKR2; OMA:PROKR2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_144773

NM_144944

RefSeq (protein)

NP_658986

NP_659193

Location (UCSC)Chr 20: 5.3 – 5.32 MbChr 2: 132.18 – 132.23 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Prokineticin receptor 2 (PKR2), is a G protein-coupled receptor encoded by the PROKR2 gene in humans.[5]

Function

Prokineticins are secreted proteins that can promote angiogenesis and induce strong gastrointestinal smooth muscle contraction. The protein encoded by this gene is an integral membrane protein and G protein-coupled receptor for prokineticins. The encoded protein is similar in sequence to GPR73, another G protein-coupled receptor for prokineticins.[5]

Mutations in the PROKR2 (also known as KAL3) gene have been implicated in hypogonadotropic hypogonadism and gynecomastia.[6]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000101292Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000050558Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b "Entrez Gene: PROKR2 prokineticin receptor 2".
  6. ^ Narula HS, Carlson HE (November 2014). "Gynaecomastia--pathophysiology, diagnosis and treatment". Nature Reviews. Endocrinology. 10 (11): 684–98. doi:10.1038/nrendo.2014.139. PMID 25112235.

Further reading

  • Lin DC, Bullock CM, Ehlert FJ, Chen JL, Tian H, Zhou QY (May 2002). "Identification and molecular characterization of two closely related G protein-coupled receptors activated by prokineticins/endocrine gland vascular endothelial growth factor". The Journal of Biological Chemistry. 277 (22): 19276–80. doi:10.1074/jbc.M202139200. PMID 11886876.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  • Soga T, Matsumoto Si, Oda T, Saito T, Hiyama H, Takasaki J, Kamohara M, Ohishi T, Matsushime H, Furuichi K (December 2002). "Molecular cloning and characterization of prokineticin receptors". Biochimica et Biophysica Acta. 1579 (2–3): 173–9. doi:10.1016/S0167-4781(02)00546-8. PMID 12427552.
  • Battersby S, Critchley HO, Morgan K, Millar RP, Jabbour HN (May 2004). "Expression and regulation of the prokineticins (endocrine gland-derived vascular endothelial growth factor and Bv8) and their receptors in the human endometrium across the menstrual cycle". The Journal of Clinical Endocrinology and Metabolism. 89 (5): 2463–9. doi:10.1210/jc.2003-032012. PMID 15126578.
  • Pasquali D, Rossi V, Staibano S, De Rosa G, Chieffi P, Prezioso D, Mirone V, Mascolo M, Tramontano D, Bellastella A, Sinisi AA (September 2006). "The endocrine-gland-derived vascular endothelial growth factor (EG-VEGF)/prokineticin 1 and 2 and receptor expression in human prostate: Up-regulation of EG-VEGF/prokineticin 1 with malignancy". Endocrinology. 147 (9): 4245–51. doi:10.1210/en.2006-0614. PMID 16763065.
  • Dodé C, Teixeira L, Levilliers J, Fouveaut C, Bouchard P, Kottler ML, Lespinasse J, Lienhardt-Roussie A, Mathieu M, Moerman A, Morgan G, Murat A, Toublanc JE, Wolczynski S, Delpech M, Petit C, Young J, Hardelin JP (October 2006). "Kallmann syndrome: mutations in the genes encoding prokineticin-2 and prokineticin receptor-2". PLoS Genetics. 2 (10): e175. doi:10.1371/journal.pgen.0020175. PMC 1617130. PMID 17054399.{{cite journal}}: CS1 maint: unflagged free DOI (link)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.