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Protein Page:
PROKR2 (human)

Overview
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.
Protein type: GPCR, family 1; Membrane protein, integral; Receptor, GPCR; Membrane protein, multi-pass
Cellular Component: integral to membrane; plasma membrane
Molecular Function: neuropeptide Y receptor activity
Biological Process: circadian rhythm; neuropeptide signaling pathway
Reference #:  Q8NFJ6 (UniProtKB)
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
Molecular weight: 43,996 Da
Basal Isoelectric point: 9.04  Predict pI for various phosphorylation states
Select Structure to View Below

PROKR2

Protein Structure Not Found.


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Modification Sites and Domains  

Modification Sites in Parent Protein, Orthologs, and Isoforms  
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       human

 
0 1 S362-p SQRGSKSsADLDLRt
0 1 T369-p sADLDLRtNGVPtTE
0 1 T374-p LRtNGVPtTEEVDCI
  mouse

 
S359 SHYGSKSSADLDLKT
T366 SADLDLKTSGVPATE
A371 LKTSGVPATEEVDCI
  rat

 
S361 SHYGSKSSADLDLKT
T368 SADLDLKTSGVPATE
A373 LKTSGVPATEEVDCI
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