|Application ||WB, IP|
|Calculated MW||84640 Da|
|Application & Usage||Western blot (at 0.5-1 µg/ml) and immunoprecipitation (4-8 µg/ml). However, the optimal conditions should be determined individually.|
|Other Names||IKK-alpha, IKKA, IKK-A, IKBKA, NFKBIKA, TCF16, CHUK, IKK1|
|Formulation||100 µg (0.5 mg/ml) Protein A purified rabbit anti-IKKα polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 50% glycerol, 1% BSA, 0.02% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||IKKalpha/IKK-1 Antibody 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.
IKKα (IkB kinase-α or IKK-1) is part of a large protein complex responsible for the inducible phosphorylation of IkB proteins. Human IKK-α is an 85 kDa peptide that has been shown to activate NFkB by phosphorylation of IkB proteins. IKKα interacts with its upstream kinase, NIK, and its downstream substrate, the IkB proteins. Mutations of IKKα in its kinase domain lead to a dominant-negative phenotype that suppresses TNF-α and IL-1β induced NFkB activation.
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