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FLASH GENE
Symbol S1PR2 contributors: mct - updated : 25-02-2016
HGNC name sphingosine-1-phosphate receptor 2
HGNC id 3169
Corresponding disease
DFNB68 neurosensory deafness 68
Location 19p13.2      Physical location : 10.332.108 - 10.341.948
Synonym name
  • bioactive lipid sphingosine 1-phosphate 2
  • S1P receptor EDG5
  • endothelial differentiation, sphingolipid G-protein-coupled receptor, 5
  • Synonym symbol(s) H218, AGR16, H218, LPB2, S1P2, EDG-5, EDG5, Gpcr13,
    DNA
    TYPE functioning gene
    STRUCTURE 10.37 kb     2 Exon(s)
    MAPPING cloned Y linked N status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    2 - 3589 38 353 - 2004 15138255
    EXPRESSION
    Type restricted
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Lymphoid/Immunelymph node    
    Reproductivefemale systemuterus   
    cells
    SystemCellPubmedSpeciesStageRna symbol
    Nervousneuroectodermal cell Mus musculusFetal
    Nervousneuron Mus musculusFetal
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
  • seven transmembrane domains (7TM)
  • HOMOLOGY
    interspecies homolog to rattus Gpcr 13
    homolog to murine Edg5
    ortholog to Drosophila Mbf1
    ortholog to C.elegans H21p03.1
    Homologene
    FAMILY
  • G protein-coupled receptor family
  • EDG family
  • CATEGORY receptor membrane G
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,nucleus
    basic FUNCTION
  • participating in sphingosine 1-phosphate-induced cell proliferation, survival and transcriptional activation
  • activator of MAPK
  • playing a dominant role in the coupling of S1P to phospholipse D in myoblasts and that the down-regulation of the receptor subtype is responsible for the specific uncoupling of S1P signalling to PLD in myotubes
  • having redundant or cooperative functions for the development of a stable and mature vascular system during embryonic development
  • modulate intracellular Ca2+ homeostasis
  • role of S1PR2 as a potent regulator of the inflammatory response within vascular endothelium
  • play a critical role in regulating human mast cell functions, including degranulation and cytokine and chemokine release
  • role for a migration inhibitory receptor, S1PR2, in promoting GC B-cell confinement to Germinal centers (GCs)
  • while S1PR1 mediates chemoattraction toward S1P in bone marrow, where S1P concentration is low, S1PR2 mediates chemorepulsion in blood, where the S1P concentration is high
  • S1PR1 and S1PR2 function potentially cooperatively to regulate vascular development
  • S1PR1, S1PR2 coordinately induce mesenchymal cell migration through S1P activation of complementary kinase pathways
  • S1PR1 and S1PR2 cooperatively regulate embryonic vascular patterning and endothelial barrier function by influencing the organization of F-actin and tight junction proteins
  • plays a key role in the permeability and inflammatory responses of the vascular endothelium during endotoxemia
  • critical in the immune, nervous, metabolic, cardiovascular, musculoskeletal, and renal systems
  • migration of macrophages, toward S1P is determined by the S1P receptor expression profile, with S1PR1/S1PR3 stimulating and S1PR2 attenuating migration
  • S1PR2 and S1PR3, likely are collectively essential mediators of eyelid closure during development
  • link between S1PR2 signaling and BBB (blod-brain-barriere) polarity, that implicate S1PR2 in sex-specific patterns of disease during CNS autoimmunity
  • in S1P-induced migration of human bone marrow-derived mesenchymal stem cells (BMSCs), S1PR2 mediates the inhibition of migration
  • S1PR1 and S1PR2 play crucial roles in hyperglycemia-induced endothelial cell dysfunction
  • inhibition of endothelial S1PR2 signaling diminishes endothelial senescence-associated functional impairments and atherogenic stimuli-induced endothelial activation
  • modulates endotoxin-induced inflammation in endothelium
  • is a critical receptor in macrophage, impairs phagocytosis and antimicrobial defense in the pathogenesis of sepsis
  • plays a critical role in the induction of cerebrovascular permeability, development of intracerebral haemorrhage and neurovascular injury in experimental stroke
  • in the surrounding normal cells plays a positive role in the apical elimination of the transformed cells, and a role in epithelial defense against cancer (EDAC)
  • can exert its influence on inner ear function through regulation of inner ear fluid homeostasis or through changes in expression of other essential inner ear proteins
  • CELLULAR PROCESS cell life, proliferation/growth
    nucleotide, transcription, regulation
    PHYSIOLOGICAL PROCESS
    text positive control of cell proliferation
    PATHWAY
    metabolism
    signaling signal transduction
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • is a receptor for RTN4 repressing synaptic plasticity
  • important role for S1PR2 and S1PR3 in S1P/HGF-mediated EC barrier responses that are associated with their complex formation with ITGB4
  • cell & other
  • lipid
  • REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) DFNB68
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    significantly decreased by 73p100 in abdominal aortic aneurysms (AAAs) compared with the control group
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    neurosensorialear 
    it is possible that targeted stimulation of S1PR2 can be used to attenuate the harmful effects of ototoxic drugs on hair cells within the human inner ear
    miscelleaneousvascular 
    is a novel therapeutic target for vascular disorders
    ANIMAL & CELL MODELS
  • in the previously reported S1pr2-/- mice, stria vascularis abnormalities, organ of Corti degeneration, and profound hearing loss were observed