Prokineticin receptor 2: Difference between revisions

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== Further reading ==
== Further reading ==
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* {{cite journal | vauthors = Lin DC, Bullock CM, Ehlert FJ, Chen JL, Tian H, Zhou QY | title = Identification and molecular characterization of two closely related G protein-coupled receptors activated by prokineticins/endocrine gland vascular endothelial growth factor | journal = The Journal of Biological Chemistry | volume = 277 | issue = 22 | pages = 19276–80 | date = May 2002 | pmid = 11886876 | doi = 10.1074/jbc.M202139200 }}
* {{cite journal | vauthors = Lin DC, Bullock CM, Ehlert FJ, Chen JL, Tian H, Zhou QY | title = Identification and molecular characterization of two closely related G protein-coupled receptors activated by prokineticins/endocrine gland vascular endothelial growth factor | journal = The Journal of Biological Chemistry | volume = 277 | issue = 22 | pages = 19276–80 | date = May 2002 | pmid = 11886876 | doi = 10.1074/jbc.M202139200 | url = http://www.jbc.org/content/277/22/19276.full.pdf }}
* {{cite journal | vauthors = Soga T, ((Matsumoto Si)), Oda T, Saito T, Hiyama H, Takasaki J, Kamohara M, Ohishi T, Matsushime H, Furuichi K | title = Molecular cloning and characterization of prokineticin receptors | journal = Biochimica et Biophysica Acta | volume = 1579 | issue = 2-3 | pages = 173–9 | date = December 2002 | pmid = 12427552 | doi = 10.1016/S0167-4781(02)00546-8 }}
* {{cite journal | vauthors = Soga T, ((Matsumoto Si)), Oda T, Saito T, Hiyama H, Takasaki J, Kamohara M, Ohishi T, Matsushime H, Furuichi K | title = Molecular cloning and characterization of prokineticin receptors | journal = Biochimica et Biophysica Acta | volume = 1579 | issue = 2-3 | pages = 173–9 | date = December 2002 | pmid = 12427552 | doi = 10.1016/S0167-4781(02)00546-8 }}
* {{cite journal | vauthors = Battersby S, Critchley HO, Morgan K, Millar RP, Jabbour HN | title = 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 | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 89 | issue = 5 | pages = 2463–9 | date = May 2004 | pmid = 15126578 | doi = 10.1210/jc.2003-032012 }}
* {{cite journal | vauthors = Battersby S, Critchley HO, Morgan K, Millar RP, Jabbour HN | title = 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 | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 89 | issue = 5 | pages = 2463–9 | date = May 2004 | pmid = 15126578 | doi = 10.1210/jc.2003-032012 }}
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{{NLM content}}
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{{G protein-coupled receptors}}
{{G protein-coupled receptors}}
[[Category:G protein coupled receptors]]
[[Category:G protein-coupled receptors]]

Latest revision as of 07:15, 10 January 2019

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Prokineticin receptor 2 (PKR2), is a G protein-coupled receptor encoded by the PROKR2 gene in humans.[1]

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.[1]

Mutations in the PROKR2 (also known as KAL3) gene have been implicated in hypogonadotropic hypogonadism and gynecomastia.[2]

See also

References

  1. 1.0 1.1 "Entrez Gene: PROKR2 prokineticin receptor 2".
  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

External links

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