Prokineticin receptor 2
From Wikipedia, the free encyclopedia
PROKR2 | |||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Identifiers | |||||||||||||||||
Aliases | PROKR2, GPR73L1, GPR73b, GPRg2, HH3, KAL3, PKR2, dJ680N4.3, prokineticin receptor 2 | ||||||||||||||||
External IDs | MGI: 2181363 HomoloGene: 16368 GeneCards: PROKR2 | ||||||||||||||||
|
|||||||||||||||||
RNA expression pattern | |||||||||||||||||
![]() |
|||||||||||||||||
More reference expression data | |||||||||||||||||
Orthologs | |||||||||||||||||
Species | Human | Mouse | |||||||||||||||
Entrez |
|
|
|||||||||||||||
Ensembl |
|
|
|||||||||||||||
UniProt |
|
|
|||||||||||||||
RefSeq (mRNA) |
|
|
|||||||||||||||
RefSeq (protein) |
|
|
|||||||||||||||
Location (UCSC) | Chr 20: 5.3 – 5.31 Mb | Chr 2: 132.34 – 132.39 Mb | |||||||||||||||
PubMed search | [1] | [2] | |||||||||||||||
Wikidata | |||||||||||||||||
View/Edit Human | View/Edit Mouse |
Prokineticin receptor 2 (PKR2), is a G protein-coupled receptor encoded by the PROKR2 gene in humans.[3]
Function[edit]
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.[3]
Mutations in the PROKR2 (also known as KAL3) gene have been implicated in hypogonadotropic hypogonadism and gynecomastia.[4]
See also[edit]
References[edit]
- ^ "Human PubMed Reference:".
- ^ "Mouse PubMed Reference:".
- ^ a b "Entrez Gene: PROKR2 prokineticin receptor 2".
- ^ 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[edit]
- 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.
- 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.
External links[edit]
- GeneReviews/NCBI/NIH/UW entry on Kallmann syndrome
- "Prokineticin Receptors: PKR2". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology.
![]() |
This transmembrane receptor-related article is a stub. You can help Wikipedia by expanding it. |
This article incorporates text from the United States National Library of Medicine, which is in the public domain.