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FLASH GENE
Symbol JUND contributors: mct/npt - updated : 26-09-2013
HGNC name jun D proto-oncogene
HGNC id 6206
Location 19p13.11      Physical location : 18.390.562 - 18.392.432
Synonym name
  • transcription factor JUND
  • JunD-FL isoform
  • activator protein 1
  • Synonym symbol(s) AP-1
    DNA
    TYPE functioning gene
    STRUCTURE 1.87 kb     1 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked   status confirmed
    Map pter - D19S411 - D19S410 - D19S212 - (JUND - COMP ) - D19S460 - D19S215 - D19S815 - cen
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    1 - 1890 35.2 347 - 2008 18071306
    EXPRESSION
    Type widely
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Hearing/Equilibriumear   highly
    Lymphoid/Immunetonsils   highly
    Reproductivefemale systemovary  highly
    Respiratorylung    
    Urinarykidney   highly
    Visualeyelens   
     eyeretina   
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
  • a basic leucine zipper (bZIP) domain
  • mono polymer heteromer , dimer
    HOMOLOGY
    intraspecies homolog to jun protooncogene D
    Homologene
    FAMILY
  • activated protein-1 family of transcription factors
  • bZIP family
  • Jun subfamily
  • CATEGORY transcription factor , protooncogene
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,nucleus,chromatin/chromosome
    basic FUNCTION
  • protecting cells from TP53-dependent senescence and apoptosis
  • reducing tumor angiogenesis by protecting cells from oxidative stress
  • major determinant of macrophage activity, directly regulating the secretion of IL6, IL10, TNF1 in primary macrophages
  • cannot functionally replace Jun in regulating fibroblast proliferation
  • functioning as a negative regulator of cell proliferation and protecting against apoptosis and oxidative stress
  • is a mediator of the profibrotic effects of TGFB1
  • could control the expression of proteins involved in signal transduction, cell survival and metabolism
  • presence of a common oncogenic cascade initiated by FOSL2/JUND in CCR4-expressing mature T-cell malignancies
  • regulates a wide range of cellular processes including proliferation, differentiation, and apoptosis
  • major gatekeeper against oxidative stress
  • provides protection in aging-induced endothelial dysfunction and may represent a novel target to prevent reactive oxygen species-driven vascular aging
  • CELLULAR PROCESS nucleotide, transcription
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • forming heterodimers with JUN, JUNB, JUND, FOS, FOSB to form the transcription factor AP1 major target of mitogen-activated signal transduction pathway, role antiapoptotic (protection from senescence)
  • heterodimer comprised of JUN and FOS proteins
  • INTERACTION
    DNA binds DNA as a dimer
    RNA
    small molecule
    protein
  • inhibitor of RHOH gene expression bound to the proximal region of the CDK4-promoter (transcriptional repression of CDK4 by JUND was mediated through an AP-1 binding site within this proximal sequence of the CDK4-promoter)
  • polyamines modulate the stability of JUND mRNA in intestinal epithelial cells through ELAVL1 and HNRNPD
  • inhibitor of RHOH gene expression
  • proximal DNA elements within the GAST promoter mediate interactions between JUND, which induces GAST gene expression and MEN1, which suppresses JUND-mediated activation
  • NFE2 modulates JUND binding to the GCM1 promoter via acetylation
  • MEN1–JUND interaction blocks JUN N-terminal kinase (JNK)-mediated JUND phosphorylation and suppresses JUND-induced transcription
  • can promote positive signals transduced through PIM1
  • BMP4 regulated JUND activity at the transcriptional regulation and post-translational modification levels
  • associated with the LILRB1 distal promoter, and depletion of JUND led to a decrease in distal promoter transcript, indicating an activating role for JUND in regulation of LILRB1 transcription
  • BAG3 stabilized JUND mRNA, which was, at least in part, responsible for the promotion of serum starvation mediated-growth inhibition by BAG3
  • cell & other
    REGULATION
    induced by ligand induced
    inhibited by MEN1
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    with CKM, myogenin, myosin, in muscle wasting of human cachexia
    constitutional     --over  
    in systemic sclerosis
    Susceptibility to glomerulonephritis
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    immunologyinflammatory 
    inhibition of JUND acting as a possible new therapeutic strategy for diseases characterized by inflammation and macrophage activation
    ANIMAL & CELL MODELS
  • JunD(-/-) mice displayed an age-independent decline in endothelial nitric oxide release and endothelial nitric oxide synthase activity and increased mitochondrial superoxide formation and peroxynitrite levels