The NF-κB/Rel transcription factors are present in the cytosol in an inactive state complexed with the inhibitory IκB proteins. Activation occurs via phosphorylation of IκBα at Ser32 and Ser36 followed by proteasome-mediated degradation that results in the release and nuclear translocation of active NF-κB. IκBα phosphorylation and resulting Rel-dependent transcription are activated by a highly diverse group of extracellular signals including inflammatory cytokines, growth factors, and chemokines. Kinases that phosphorylate IκB at these activating sites have been identified.
Stoccaggio: Store at -20℃ Valid for 12 months. Avoid freeze / thaw cycles.
Isotipo: IgG,κ
Clonalità: Monoclonal;Recombinant
Clone: A819
Coniugazione: Unconjugated
Applicazione: WB
Diluizione: WB 1:1000-2000
Simbolo target: Phospho-IκBα (Ser36)
Ig target: EDAID;MAD;IKBA;MAD-3;NFKBI;IKB alpha;NFKBIA;EDAID2;I kappa B alpha;IkappaBalpha;I-kappa-B-alpha;IKBalpha;IkB-alpha;MAD 3;NF kappa B inhibitor alpha;MAD3;alpha;Major histocompatibility complex enhancer-binding protein MAD3;NF-kappa-B inhibitor alpha;Nuclear factor of kappa light chain gene enhancer in B cells;Nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha;nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor;pIκBα
Area di ricerca:Signal Transduction;Epigenetics and Nuclear Signaling;Cancer;Immunology
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