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FLASH GENE
Symbol ARID3A contributors: mct - updated : 03-09-2014
HGNC name AT rich interactive domain 3A (BRIGHT-like)
HGNC id 3031
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
9 - 2823 - 593 - 2002 11812999
EXPRESSION
Type widely
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestiveintestinelarge intestinecolon highly
Nervousbraindiencephalonthalamus highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Connectivebonesubchondral  
Muscularstriatumskeletal  
cells
SystemCellPubmedSpeciesStageRna symbol
Lymphoid/ImmuneB cell Homo sapiens
cell lineage in B lymphocyte lineage cells
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a functional nuclear localization signal to the N-terminal region of REKLES, a domain conserved within ARID3 paralogues
  • one DNA binding protein containing one AT/rich interaction domain (ARID)
  • one nucleosome assembly protein (NAP) domain
  • AAs within the C terminal REKLES domain containing its nuclear export signal, whose regulation is primarily responsible for its shuttling
  • HOMOLOGY
    interspecies homolog to murine Bright (B cell regulator of IgH transcription)
    homolog to Drosophila dead ringer
    intraspecies paralog to DRIL2
    Homologene
    FAMILY ARID (AT-rich interaction domain) family
    CATEGORY immunity/defense , regulatory , DNA associated , protooncogene
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm
    intracellular,nucleus,nucleoplasm
    text
  • actively shuttles between the nucleus and the cytoplasm in a CRM1-dependent manner
  • basic FUNCTION
  • playing a role in embryonic patterning, cell lineage gene regulation, cell cycle control, transcriptional regulation and possibly in chromatin structure modification
  • regulation of its cellular localization appears to be required for its function
  • nuclear matrix-associated transcription factor that stimulates immunoglobulin heavy chain (IgH) expression and Cyclin E1/E2F-dependent cell cycle progression
  • contributor to accessibility of the IgH enhancer
  • B cell-specific, matrix association (or attachment) region-binding transcriptional regulator of immunoglobulin heavy chain genes and of E2F1-dependent cell cycle progression
  • A+T-rich interaction domain protein, originally discovered in B lymphocyte lineage cells
  • activator of immunoglobulin heavy-chain transcription and proto-oncogene
  • transcriptional regulator required to program both hematopoietic stem cell and lineage-specific differentiation
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA binding to promoter proximal site
    RNA
    small molecule
    protein
  • binding partner for ID1 (shares structural similarities with ID1 and recently implicated in TGF-beta1 signaling during embryogenesis
  • B-cell-restricted factor that complexes with Bruton tyrosine kinase (BTK) and its substrate, transcription initiation factor-I (GTF2I), to activate immunoglobulin heavy chain gene transcription in the nucleus
  • transiently interacts with sumoylation enzymes, blocks calcium flux and phosphorylation of BTK and GTF2II and is then discharged from lipid rafts as a Sumo-I-modified form
  • bound to its binding sites in the CDKN1A promoter
  • LIN28B promotes fetal B lymphopoiesis through the transcription factor ARID3A
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    in lungs from patients with idiopathic pulmonary fibrosis and was regulated by TGF-beta1 in human fibroblasts
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
    hematopoietic potential of Bright(-/-) mice is markedly reduced