• IκB-α Mouse mAb(2A5)
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Upingbio

YP-Ab-04803-100UL

IκB-α Mouse mAb(2A5)

IκB-α Mouse mAb(2A5)

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  • Reaction species: Human; Mouse;Rat
  • Gene Name: NFKBIA IKBA MAD3 NFKBI
  • Protein name: NF-kappa-B inhibitor alpha
  • Molecular weight (DA): about 40kd
  • Immunogen: Synthesized peptide derived from human IκB α
  • Specificity: This antibody detects endogenous levels of IκB α at Human, Mouse,Rat
  • Composition: Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.44% sodium azide.
  • Source: Monoclonal, Mouse
  • Dilution ratio: IHC-p1:50-200 ,WB 1:1000-2000
  • Purification process: The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
  • Concentration: mg/ml
  • Storage: -20°C/1 year
  • Other Names: NF-kappa-B inhibitor alpha (I-kappa-B-alpha) (IkB-alpha) (IkappaBalpha) (Major histocompatibility complex enhancer-binding protein MAD3)
  • Background: This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease. [provided by RefSeq, Aug 2011],
  • Function: disease:Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection.,function:Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to tranlocate to the nucleus and activate transcription.,induction:Induced in adherent monocytes.,online information:NFKBIA mutation
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