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FLASH GENE
Symbol JUNB contributors: mct/shn - updated : 20-12-2018
HGNC name jun B proto-oncogene
HGNC id 6205
Location 19p13.2      Physical location : 12.902.309 - 12.904.124
Synonym name
  • activator protein 1
  • transcription factor jun-B
    • Synonym symbol(s) AP-1
    DNA
    TYPE functioning gene
    STRUCTURE 1.82 kb     1 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked N status confirmed
    Map pter - D19S1165 - D19S221 - JUNB - D19S914 - D19S840 - cen
    regionally located localized in the psoriasis susceptibility region PSORS6
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    1 - 1832 - 347 - 2008 18628455
    EXPRESSION
    Type ubiquitous
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Cardiovascularheart    
    Digestiveliver   highly
    Nervousbrain   highly
     nervecranial nerve  highly
     spinal cord    
    Reproductivefemale systemuteruscervix highly
    Respiratorylung   highly
    Urinarykidney   highly
    tissue
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Blood / Hematopoieticbone marrow   
    Connectiveadipose  highly
    Connectivebone   
    Muscularstriatumcardiac  
    Nervouscentral   
    cell lineage erythroid
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES basic
    STRUCTURE
    motifs/domains
  • basic leucine zipper (bZIP) domain
    • conjugated ubiquitinated
    mono polymer heteromer , dimer
    HOMOLOGY
    interspecies ortholog to Junb, Mus musculus
    ortholog to Junb, Rattus norvegicus
    ortholog to JUNB, Pan troglodytes
    Homologene
    FAMILY
  • AP-1 family
  • BZIP family
  • JUN subfamily
    • CATEGORY transcription factor , protooncogene
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,nucleus,chromatin/chromosome
    intracellular,nucleus,nucleolus
    basic FUNCTION
  • repressor of CCND1 promoter
  • regulator of erythroid differentiation
  • hypoxia-responsive transcription factor, absolutely required for VEGF regulation in a cell-type-independent manner
  • a key transcriptional regulator of myelopoiesis and a potential tumor suppressor gene
  • a positive regulator controlling primarily osteoblast as well as osteoclast activity
  • critical regulator of intrinsic mast cell functions including cross-talk with endothelial cells
  • essential upstream regulator of p16 and contributes to maintain cell senescence that blocks malignant transformation of transient amplifying cells
  • apparently plays an important role in controlling prostate carcinogenesis
  • critical regulator of T cell function and a transcriptional activator of various cytokine genes, such as IL2, IL4, and IL10
  • REL and JUNB cooperatively regulate FOXP3 expression by modulating the chromatin architecture of FOXP3 promoter region
  • GRN growth factor, JUNB, and MYOD1 transcription factor form a regulatory loop and act in concert in the course of myogenesis
  • a critical role in the epithelial-mesenchymal transition and profibrotic responses to TGF-beta
  • provides important input in setting the transcriptional program of the epithelial-mesenchymal transition and profibrotic responses to TGF-beta
    • CELLULAR PROCESS cell life, differentiation
    nucleotide, transcription
    PHYSIOLOGICAL PROCESS circadian
    PATHWAY
    metabolism
    signaling
    a component
  • forming heterodimers with JUN, JUND, FOS, FOSB to form the transcription factor AP1 major target of mitogen-activated signal transduction pathway
  • REL and JUNB cooperatively enhance FOXP3 expression during induced regulatory T cell differentiation
  • BATF forms a heterodimeric complex with JUNB and JUN, induced upregulation of matrix-degrading enzymes and downregulation of cartilage matrix molecules in chondrocytes
    • INTERACTION
    DNA
    RNA
    small molecule
  • conjugated with small ubiquitin-like modifier (SUMO) on lysine 237
    • protein
  • B-ATF
  • c-Jun NH2-terminal kinase, JNK
  • Nrf2 and Nrf1
  • Smad3 and Smad4
  • estrogen receptor alpha, ERalpha
  • BRCA1
  • BCL-6
  • c-Fos and LRF-1
  • c-Jun
  • NFATC2 and JUNB cooperatively regulate IL31 gene expression in CD4+ T cells in health and disease
  • BATF/JUNB and BATF/JUN complexes play important roles in osteoarthritic cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes
  • N4BP1 controls the proper function of keratinocytes and neutrophils by negatively regulating JUNB, FOSB, and CXCL1, respectively, and that is critical for psoriasis prevention
    • cell & other
    REGULATION
    activated by erythropoietin induced
    hypoxia-induced NFKB
    induced by ligand induced
    light in the suprachiasmatic nucleus
    in response to hypoxia and required for VEGF expression
    Other phosphorylated and inactivated by CDC2, in mitotic and early G1 cells
    sumoylation of JUNB regulates its ability to induce cytokine gene transcription and likely plays a critical role in T cell activation
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    with JUN in Hodgkin lymphoma cells
    constitutional     --low  
    in epidermal keratinocytes of psoriatic lesions
    constitutional        
    affects VEGF expression resulting in impaired neovascularization (in tumor)
    tumoral     --low  
    in patients with chronic myelogenous leukemia, due aberrant DNA methylation of its promoter, but downregulated in advanced phase CML through a mechanism independent from DNA methylation
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cancerangiogenesis 
    for anti-angiogenic tumor therapies
    cancer  
    new target for cancer prevention and therapy
    ANIMAL & CELL MODELS
  • Transgenic mice specifically lacking JunB expression in the myeloid lineage develop a transplantable myeloproliferative disease eventually progressing to blast crisis and mice reconstituted with ES cell-derived junB-/- fetal liver cells also develop a myeloproliferative disease
  • JunBDelta/Delta mice are viable, but develop severe low turnover osteopenia caused by apparent cell-autonomous osteoblast and osteoclast defects before a chronic myeloid leukemia-like disease
  • mice with specific inactivation of Junb in the macrophage-osteoclast lineage develop an osteopetrosis-like phenotype with increased bone mass and reduced numbers of osteoclasts
  • inducible epidermal deletion of JunB and c-Jun in adult mice leads to a phenotype resembling the histological and molecular hallmarks of psoriasis, including arthritic lesions
  • Depletion of JunB by siRNA abrogates TGF-&
    • 946;-induced disruption of cell-cell junctions, formation of actin fibers, focal adhesions, and expression of fibrotic proteins