Description
Protocol
Available protocols: ELISA+
Specificity / Sensitivity
PathScan
Species Reactivity: Human, Mouse
Background
The NF-κB/Rel transcription factors are present in the cytosol in an inactive state complexed with the inhibitory IκB proteins (1-3). 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 (3-7). 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 (8).
Alternate Names
EDAID2; I-kappa-B-alpha; IkappaBalpha; IkB-alpha; IKBA; MAD-3; MAD3; Major histocompatibility complex enhancer-binding protein MAD3; NF-kappa-B inhibitor alpha; NFKB inhibitor alpha; NFKBI; NFKBIA; nuclear factor of kappa light chain gene enhancer in B-cells; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha
