|Calculated MW||35609 Da|
|Other Names||NF-kappa-B inhibitor alpha, I-kappa-B-alpha, IkB-alpha, IkappaBalpha, Major histocompatibility complex enhancer-binding protein MAD3, NFKBIA, IKBA, MAD3, NFKBI|
|Target/Specificity||A phospho specific peptide corresponding to residues surrounding Serine 32 of human IkappaB-alpha was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||IkappaB-alpha Antibody Phospho (S32) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||IKBA, MAD3, NFKBI|
|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 translocate to the nucleus and activate transcription.|
|Cellular Location||Cytoplasm. Nucleus. Note=Shuttles between the nucleus and the cytoplasm by a nuclear localization signal (NLS) and a CRM1-dependent nuclear export.|
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Provided below are standard protocols that you may find useful for product applications.
The NF-kappaB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IkappaB-alpha protein (1-5). In response to many different NF-kappaB-inducing agents including T-cell mitogens, proinflammatory cytokines, and viral transactivators, the inhibitory IkappaB-alpha is rapidly phosphorylated and degraded (2). Phosphorylation of IkappaB-alpha at Ser32 and Ser36 has been shown to stimulate conjugation with ubiquitin and subsequent degradation of IkappaB-alpha (3). Activation of NF-kappaB can also be achieved after tyrosine phosphorylation of IkappaBalpha at tyrosine 42, an event that also ultimately leads to the dissociation of NF-kappaB and IkappaBalpha (4). Phosphorylation of IkappaB-alpha at Ser32 and Tyr42 is critical for activation of NF-kappaB, which then translocates to the nucleus and induces transcription of genes that protect organism (1-5).
1. Traenckner E.B., et al. EMBO J. 14: 2876-83, 1995 2. Brockman J.A., et al. Mol. Cell. Biol. 15(5): 2809-18, 1995 3. Chen Z.J., et al. Cell 84(6): 853-62, 1996 4. Witherow DS., et al. Proc Natl Acad Sci USA. 101(23):8603-8607, 2004 5. Brown K., et al. Science 267(5203): 1485-8, 1995
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