IkB alpha, phosphorylated (Ser32/Ser36) (NF-kappa-B Inhibitor alpha, I-kappa-B-alpha, IkB-alpha, IkappaBalpha, Major Histocompatibility Complex Enhancer-binding Protein MAD3, NFKBIA, IKBA, MAD3, NFKBI)

The NF-kB/Rel transcription factors are present in the cytosol in an inactive state complexed with the inhibitory IkB proteins. Activation of IkB-a occurs through both serine and tyrosine phosphorylation events. Activation through phosphorylation at Ser32 and Ser36 is followed by proteasome-mediated degradation, resulting in the release and nuclear translocation of active NF-kB. This pathway of IkB-a regulation occurs in response to various NF-kB-activating agents, such as TNFa, interleukins, LPS, and irradiation. An alternative pathway for IkB-a regulation occurs through tyrosine phosphorylation of Tyr42 and Tyr305. Tyr42 is phosphorylated in response to oxidative stress and growth factors. This phosphorylation can lead to degradation of IkB-a and NF-kB-activation. In contrast, Tyr305 phosphorylation by c-Abl has been implicated in IkB-a nuclear translocation and inhibition of NF-kB-activation. Thus, tyrosine phosphorylation of IkB-a may be an important regulatory mechanism in NF-kB signaling.\n\nApplications:\nSuitable for use in Immunohistochemistry. Other applications not tested.\n\nRecommended Dilution:\nImmunohistochemistry (Formalin fixed paraffin embedded): 1:50-1:100\nOptimal dilutions to be determined by the researcher.\n\nStorage and Stability:\nMay be stored at 4 degrees C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

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