|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||84640 Da|
|Other Names||Inhibitor of nuclear factor kappa-B kinase subunit alpha, I-kappa-B kinase alpha, IKK-A, IKK-alpha, IkBKA, IkappaB kinase, Conserved helix-loop-helix ubiquitous kinase, I-kappa-B kinase 1, IKK1, Nuclear factor NF-kappa-B inhibitor kinase alpha, NFKBIKA, Transcription factor 16, TCF-16, CHUK, IKKA, TCF16|
|Target/Specificity||A synthetic peptide corresponding to residues in the N-term of human IKK-alpha was used as 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||IKK alpha Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Serine kinase that plays an essential role in the NF- kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11). Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa- B RelB-p52 complexes. In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Participates also in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilizing MAP3K14/NIK. Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities. Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP. Additionally, phosphorylates the CREBBP-interacting protein NCOA3. Also phosphorylates FOXO3 and may regulate this pro-apoptotic transcription factor (PubMed:15084260).|
|Cellular Location||Cytoplasm. Nucleus. Note=Shuttles between the cytoplasm and the nucleus|
|Tissue Location||Widely expressed.|
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Provided below are standard protocols that you may find useful for product applications.
IKK-alpha (I-Kappa-B kinase-alpha) is a member of the IKK complex which is composed of IKK-alpha, IKK-beta, IKK-gamma and IKAP (1-2). Phosphorylation of I-Kappa-B on a serine residue by the IKK complex frees NF-kB from I-Kappa-B and marks it for degradation via ubiquination. Activation of NFKB by TNF requires phosphorylation of IKK-alpha at threonine 23 and serine 176 by AKT1 and NIK respectively (3). It has been demonstrated that IKK-alpha can accumulate in the nucleus after cytokine exposure (4). In the nucleus IKK-alpha interacts with CREB-binding protein in conjunction with RELA to be recruited to the NF-kappa-B-responsive promoters in order to mediate the cytokine-induced phosphorylation and subsequent acetylation of specific residues in histone H3 (5).
1. Zandi, E. et al. Cell 91: 243-252, 1997. 2. Scheidereit, C. Nature 395: 225-226, 1998. 3. Ozes, O. N. et al. Nature 401: 82-85, 1999. 4. Anest, V. et al. Nature 423: 659-663, 2003. 5. Yamamoto, Y. et al. Nature 423: 655-659, 2003.
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