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FLASH GENE
Symbol BEX2 contributors: mct/npt - updated : 20-03-2018
HGNC name brain expressed X-linked 2
HGNC id 30933
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
HOMOLOGY
interspecies ortholog to murine Bex2
intraspecies paralog to BEX1
Homologene
FAMILY
  • Brain Expressed X-linked gene family
    • CATEGORY regulatory , signaling
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    intracellular,nucleus
    basic FUNCTION
  • may be a signaling adaptor molecule
  • can enhance the transcriptional activity of LMO2
  • may act as a specific regulator during embryonic development by modulating the transcriptional activity of a novel E-box sequence-binding complex that contains BEX2, LM2, NSCL2 and LDB1
  • is implicated in oligodendroglioma biology
  • has a functional interplay with JUN/JNK and RELA in breast cancer
  • may be an important player during the development of glioma
  • contributes to glioma development by regulating the JUN NH2-terminal kinase pathway
  • regulates the invasion/migration ability of glioma cells
  • increased BEX2 expression led to enhanced NFKB1 signaling as well as cell proliferation
  • while BEX1 and NGFRAP1 act as tumor suppressors, BEX2 seems to act as an oncogene
  • BEX2 promotes colorectal cancer cell proliferation via the JNK/JUN pathway
    • CELLULAR PROCESS nucleotide, transcription, regulation
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • component of a DNA-binding protein complex
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with LMO2
  • BEX2 promoted the progression of glioma by promoting cell migration and invasion, and these effects might be mediated by CDH2 and MMP2
  • BEX2 promotes proliferation of human glioblastoma cells via NFKB1 signaling pathway and BEX2 nuclear location is critical for RELA expression
  • BEX2 affects the invasion and migration ability of glioma cells by regulating CTNNB1
    • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in a subset of primary breast cancers, mediating nerve growth factor/nuclear factor-kappaB inhibition of apoptosis in breast cancer cell lines (Naderi 2007)
    tumoral     --over  
    in glioma tissues
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancerbrainglioma/neuroblstoma
    contributes to glioma development by regulating the JUN NH2-terminal kinase pathway
    cancerdigestivecolon
    BEX2 as a potential candidate target for the treatment of colorectal cancer (CRC)
    cancerbrain 
    potential target for novel therapies for ependymoma in children
    ANIMAL & CELL MODELS
  • Bex2-deficient mice were viable and fertile under laboratory growth conditions showing no obvious phenotypic abnormalities 3)