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FLASH GENE

Symbol

PROKR2

contributors: mct - updated : 02-10-2024

HGNC name	prokineticin receptor 2
HGNC id	15836

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_144773 2 - 1157 NP_658986 - 384 - 2002 11886876

EXPRESSION

Type	restricted

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Nervous brain diencephalon hypothalamus   predominantly Mus musculus   brain basal nuclei         brain diencephalon thalamus     Olfactory (smell) olfactory bulb         Mus musculus Reproductive female system placenta     highly Homo sapiens

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Epithelial secretory glandular endocrine

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	seven transmembrane helices,
	three intracellular loops (IL1–3) and the distal region of the of the third intracellular loop of PROKR2 may differentially influence receptor trafficking and G-protein coupling
	a cytoplasmic C-terminal tail, and C-terminus of PROKR2 is critical for the stability of the ARRB2-receptor complex in the presence of PROK2 ligand

mono polymer

dimer

HOMOLOGY

interspecies

homolog to murine Gpr73

Homologene

FAMILY

G protein coupled receptor family 1

CATEGORY

receptor membrane G

SUBCELLULAR LOCALIZATION

plasma membrane

basic FUNCTION	involved in the mobilization of calcium
	stimulation of phosphoinositide turnover
	activation of p44/p42 MAPK signaling pathways consistent with the effects of prokineticins on smooth muscle contraction and angiogenesis
	not necessary for suprachiasmatic nucleus cellular timekeeping or entrainment, but it is an essential link for coordination of circadian behavior and physiology by the suprachiasmatic nucleus, especially in defining the onset and maintenance of circadian night
	mediating circadian control of behavior rather than circadian timing per se
	having a dimeric structure in neutrophils (pMID: 21161321)
	PROKR1, but also PROKR2 might mediate a complementary signalling to the RET/GDNF pathway supporting proliferation/survival and differentiation of precursor cells during enteric nervous system (ENS) development
	undergoes rapid ligand-induced endocytosis, and recycles back to the plasma membrane after the removal of ligand
	involved in the regulation of sexual maturation

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

complex PROC2/PROCR2 plays a role in GNRH1 neuron development beyond olfactory bulb morphogenesis

INTERACTION

DNA

RNA

small molecule

protein	receptor for prokineticins (PROK2)
	PROK2-induced the formation of vessel-like structures by aortic endothelial cells expressing only PROKR1, and disorganized the tight junctions in hepatic sinusoidal endothelial cells expressing only PROKR2, confirming the divergent roles of these receptors
	PROK2 increases the activity of acid-sensing ion channels via the PROKR2 and protein kinase C-dependent signal pathways
	PKC activation induced PROKR2 endocytosis, however, PKC activation is not necessary for the PROK2-induced PROKR2 endocytosis
	PROK1 and PROK2 bind to two highly related G protein-coupled receptors (GPCRs), prokineticin receptor 1 (PROKR1) and prokineticin receptor 2 (PROKR2)
	PROK1, PROK2 increased blood-brain barrier (BBB) permeability, which could be prevented by PROKR1 and PROKR2 antagonists

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

KAL3

Susceptibility

to GNRH1 deficiency and failure of reproductive competency to recurrent miscarriage (RM)

Variant & Polymorphism other	PROKR2 L173R is an ancient founder mutation that was not eliminated during evolution despite being associated with GNRH1 deficiency and failure of reproductive competency
	PROKR2 (V331M) variant conferred lower risk for RM and may play protective roles in early pregnancy by altering calcium signaling and facilitating cell invasiveness

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

	Prokr2-deficient mice display vascular dysmorphology of the fetal testes
	mice lacking Prokr2 have been shown to present abnormal olfactory bulb formation as well as defects in GnRH neuron migration