KB抑制蛋白激酶α/IKK-α/IKKα/I-κB-α 抗体
规格：1mg/1ml
英文名： IKK alpha/CHUK
别名： I Kappa B Kinase Alpha; IKKalpha; IKK alpha; IkappaB kinase; IkB kinase alpha subunit; IKBKA; IKK 1; IKK A; IKK a kinase; IKK1; IKKA; Inhibitor Of Kappa Light Polypeptide Gene Enhancer In B Cells; Inh
分子量： 85kDa
储存液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce
克隆类型：Polyclonal
亚型：IgG
纯化方法：affinity purified by Protein A
**原：KLH conjugated synthetic peptide derived from human IKK alph
交叉反应：Human, Mouse, Rat, Dog, Horse,
细胞定位：细胞核 细胞浆
KB抑制蛋白激酶α/IKK-α/IKKα/I-κB-α 抗体产品介绍：background: Nuclear factor kappa B (NFkB) is a ubiquitous transcription factor and an essential mediator of gene expression during activation of immune and inflammatory responses. IκBα mediates the expression of a great variety of genes in response to extracellular stimuli including IL1, TNF alpha, and bacterial product LPS. NFkB is associated with IkB proteins in the cell cytoplasm, which inhibit IκBα activity. IKK is a serine protein kinase, and the IKK complex contains alpha and beta subunits (IKK alpha and IKK beta). IKK alpha and IKK beta interact with each other and both are essential for NFkB activation. IKK alpha specifically phosphorylates IkBa. IKKa is expressed in variety of human tissues. 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 KB抑制蛋白激酶α/IKK-α/IKKα/I-κB-α 抗体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. Subunit: Component of the I-kappa-B-kinase (IKK) core complex consisting of CHUK, IKBKB and IKBKG; probably four alpha/CHUK-beta/IKBKB dimers are associated with four gamma/IKBKG subunits. The IKK core complex seems to associate with regulatory or adapter proteins to form a IKK-signalosome holo-complex. The IKK complex associates with TERF2IP/RAP1, leading to promote IKK-mediated phosphorylation of RELA/p65. Part of a complex composed of NCOA2, NCOA3, CHUK/IKKA, IKBKB, IKBKG and CREBBP. Part of a 70-90 kDa complex at least consisting of CHUK/IKKA, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Directly interacts with IKK-gamma/NEMO and TRPC4AP (By similarity). May interact with TRAF2. Interacts with NALP2. May interact with MAVS/IPS1. Interacts with ARRB1 and ARRB2. Interacts with NLRC5; prevents CHUK phosphorylation and kinase activity. Interacts with PIAS1; this interaction induces PIAS1 phosphorylation. Subcellular Location: Cytoplasm. Nucleus. Note=Shuttles between the cytoplasm and the nucleus. Tissue Specificity: Widely expressed. Post-translational modifications: Phosphorylated by MAP3K14/NIK, AKT and to a lesser extent by MEKK1, and dephosphorylated by PP2A. KB抑制蛋白激酶α/IKK-α/IKKα/I-κB-α 抗体Autophosphorylated. Acetylation of Thr-179 by Yersinia yopJ prevents phosphorylation and activation, thus blocking the I-kappa-B signaling pathway. DISEASE: Defects in CHUK are the cause of cocoon syndrome (COCOS) [MIM:613630]; also known as fetal encasement syndrome. COCOS is a lethal syndrome characterized by multiple fetal malformations including defective face and seemingly absent limbs, which are bound to the trunk and encased under the skin. Similarity: Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. I-kappa-B kinase subfamily. Contains 1 protein kinase domain. Gene ID: 1147 Database links: Entrez Gene: 1147 Human Entrez Gene: 309361 Rat Omim: 600664 Human SwissProt: O15111 Human SwissProt: Q60680 Mouse Unigene: 198998 Human Unigene: 3996 Mouse Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
KB抑制蛋白激酶α/IKK-α/IKKα/I-κB-α 抗体产品应用：WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （石蜡切片需做抗原修复） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
研究领域：肿瘤 **学 信号转导 细胞凋亡 转录调节因子 细胞粘附分子
储存条件： Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
来源： Rabbit
外观： Lyophilized or Liquid