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FLASH GENE
Symbol NFKBIA contributors: mct - updated : 18-03-2015
HGNC name nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha
HGNC id 7797
Corresponding disease
ADEDAID ectodermal dysplasia, anhidrotic, with T-cell immunodeficiency
Location 14q13.2      Physical location : 35.870.716 - 35.873.960
Synonym name IkappaB alpha
Synonym symbol(s) IKBA, MAD-3, IKBKIA, EVI116
DNA
TYPE functioning gene
STRUCTURE 3.24 kb     6 Exon(s)
10 Kb 5' upstream gene genomic sequence study
MAPPING cloned Y linked   status provisional
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
6 - 1579 - 317 - 2000 11106428
EXPRESSION
Type widely
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestivestomach   highly
Endocrinepancreas   highly
Lymphoid/Immunetonsils   highly
Reproductivefemale systemplacenta  highly
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • nuclear export signal NES in the N terminal domain
  • five copies of the ankyrin repeat (ankyrin region)
  • a consensus sequence for PKC phosphorylation and
  • a C terminal PEST sequence
  • HOMOLOGY
    Homologene
    FAMILY NF-Kappa B inhibitor family
    CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,cytosolic
    intracellular,nucleus
    text continuously shuttling between nucleus and cytoplasm
    basic FUNCTION
  • transcription factor of kappa light chain gene enhancer in B cells (NF-kappa B) inhibitor alpha, sequestering NFKB in the cytoplasm, inhibiting NFKB activation after modification by UBL1
  • potential role for NFKBIA as a marker of NFKB/RELA activation in the oocyte and early embryo
  • CELLULAR PROCESS cell cycle
    cell life, antiapoptosis
    nucleotide, transcription
    PHYSIOLOGICAL PROCESS
    text hypoxie stress
    PATHWAY
    metabolism
    signaling
    a component
  • complex formed with TP53 dissociates in response to apoptotic stress hypoxia
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • p65 RELA
  • NKIRAS1
  • CASP1-proteasome-dependent NFKBIA polymer degradation may contribute to cancer progression through constitutive NF-kappaB activation
  • stimulates NFKB activity by destabilizing NFKBIA protein through inducing its phosphorylation and ubiquitination
  • NFKB1 signaling pathway, which involves both NFKBIA and CHUK, plays an important role in platelet CD40 signaling, activation and aggregation in response to sCD40LG
  • omentin inhibited TNF-activated signal pathway of NFKB1 by preventing NFKB1 inhibitory protein (NFKBIA) degradation and NFKB1/DNA binding activity
  • DDRGK1 interacts with NFKBIA and regulates its stability, thereby regulates the NFKB1 transcriptional activity
  • ZBTB20 could inhibit NFKBIA transcription, govern NFKBIA protein expression, then promote NFKB1 activation, and is needed to promote full activation of TLR signaling and TLR-triggered innate immune response by selectively suppressing the suppressor NFKBIA gene transcription
  • TNFAIP8L2 inhibited the phosphorylation of AKT1, while promoting the phosphorylation of MAPK14, but had no effect on NFKBIA and ERK pathway
  • EXOC3 regulates NFKB1 transcriptional activity via the control of the phosphorylation of NFKBIA, RPS6KA2, and ERK
  • PDLIM1 negatively regulates NFKB1-mediated signaling in the cytoplasm (PDLIM1 sequestered p65 subunit of NFKB1 in the cytoplasm and suppressed its nuclear translocation in an NFKBIA-independent, but ACTN4-dependent manner
  • cell & other
    REGULATION
    Other ubiquinylated by the F box protein BTRC,component of the ubiquitin protein ligase complex (SFC) with SKP1, CUL1, RBX1, BTRC
    ASSOCIATED DISORDERS
    corresponding disease(s) ADEDAID
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in esophageal squamous cell carcinoma
    tumoral       loss of function
    in Hodgkin and Reed-Sternberg cells
    tumoral   deletion    
    in glioblastomas
    tumoral somatic mutation      
    in Hodgkin lymphoma
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS