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PROKR2
Receptor for prokineticin 2. Exclusively coupled to the G(q) subclass of heteromeric G proteins. Activation leads to mobilization of calcium, stimulation of phosphoinositide turnover and activation of p44/p42 mitogen-activated protein kinase. Defects in PROKR2 are the cause of Kallmann syndrome type 3 (KAL3); also known as hypogonadotropic hypogonadism and anosmia. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin- releasing hormone-synthesizing neurons. KAL3 patients have variable degrees of olfactory and reproductive dysfunction, but do not show any of the occasional clinical anomalies reported in Kallmann syndrome such as renal agenesis, cleft lip and/or palate, selective tooth agenesis, and bimanual synkinesis. Belongs to the G-protein coupled receptor 1 family. Note: This description may include information from UniProtKB.
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| Protein type: Receptor, GPCR; GPCR, family 1; Membrane protein, integral |
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Cellular Component: plasma membrane; integral to membrane
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Molecular Function: neuropeptide Y receptor activity
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Biological Process: circadian rhythm
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Reference #:
Q8NFJ6 (UniProtKB)
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| Alt. Names/Synonyms: dJ680N4.3; G protein-coupled receptor 73-like 1; G-protein coupled receptor 73-like 1; GPR73b; GPR73L1; GPRg2; KAL3; PK-R2; PKR2; Prokineticin receptor 2; PROKR2 |
| Gene Symbols: PROKR2 |
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Molecular weight: 43,996 Da
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Basal Isoelectric point: 9.04
Predict pI for various phosphorylation states
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