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FLASH GENE
Symbol CELSR3 contributors: mct/shn/pgu - updated : 19-09-2010
HGNC name cadherin, EGF LAG seven-pass G-type receptor 3 (flamingo homolog, Drosophila)
HGNC id 3230
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • nine cadherin motifs (CA)
  • seven transmembrane segments (7TM)
  • six EGF-like motifs
  • five Calsium-binding EGF-like domains
  • two laminin G domains (LamG)
  • a Laminin EGF-like domain
  • an hormone binding domain (HRM)
  • a GPCR proteolitic site (GPS)
    • HOMOLOGY
    interspecies ortholog to celsr3, danio rerio
    ortholog to Celsr3, Rattus norvegicus
    ortholog to Celsr3, Mus musculus
    ortholog to CELSR3, Pan troglodytes
    intraspecies homolog to EGFL2
    Homologene
    FAMILY
  • G-protein coupled receptor 2 family
  • LN-TM7 subfamily
  • Flamingo subfamily
  • part of the cadherin superfamily
    • CATEGORY unknown/unspecified , receptor membrane G
    SUBCELLULAR LOCALIZATION     plasma membrane
    basic FUNCTION
  • receptor that may have an important role in cell/cell signaling during nervous system formation
  • involved in contact-mediated communication
  • crucial in axonal tract development
  • mediates interactions between axons and guidepost cells govern axonal tract formation in mammals
  • control ability of facial branchiomotor neurons (FBM neurons) to migrate
  • controls with Celsr2 the development and the function of ependymal cilia in the epithelial lining of cerebral ventricles
  • a key regulator of ciliogenesis in the ependyma
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • mice with inactivated Celsr3 gene display selective anomalies of several major axonal fascicles implicating protocadherins in axonal development
  • null mutation of Celsr3 in mice leads to defective anterior commissure and internal capsule of the axonal tracts
  • Celsr2/Celsr3 double mutant mice display markedly impairment of ependyma and ciliogenesis leading to lethal hydrocephalus