| 產(chǎn)品編號 | bs-3236R |
| 英文名稱 | Phospho-IKK alpha (Ser180) + IKK beta (Ser181) Rabbit pAb |
| 中文名稱 | 磷酸化KB抑制蛋白激酶α/β抗體 |
| 別 名 | IKK alpha+IKK beta(phospho S180+S181); p-IKK alpha+IKK beta(phospho S180+S181); 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; Inhibitor Of Nuclear Factor Kappa B Kinase alpha Subunit; NFKBIKA; Nuclear Factor Kappa B Inhibitor Kinase alpha; Nuclear factor NF kappa B inhibitor kinase alpha; Nuclear factor NFkappaB inhibitor kinase alpha; Nuclear Factor Of Kappa Light Chain Gene Enhancer In B Cells Inhibitor; TCF16; CHUK1; CHUK; Conserved Helix Loop Helix Ubiquitous Kinase; Conserved helix loop ubiquitous kinase; I Kappa B Kinase 1; IKKA_HUMAN. |
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Specific References (2) | bs-3236R has been referenced in 2 publications.
[IF=2.47] Luo, Cheng, et al. "Kaempferol alleviates insulin resistance via hepatic IKK/NF-κB signal in type 2 diabetic rats." International Immunopharmacology 28.1 (2015): 744-750. WB ; Rat.
[IF=2.08] Fu, Juanli, et al. "Tetrachlorobenzoquinone exhibits neurotoxicity by inducing inflammatory responses through ROS-mediated IKK/IκB/NF-κB signaling."Environmental Toxicology and Pharmacology (2016). WB ; Rat.
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| 產(chǎn)品類型 | 磷酸化抗體 |
| 研究領(lǐng)域 | 腫瘤 免疫學(xué) 轉(zhuǎn)錄調(diào)節(jié)因子 細(xì)胞粘附分子 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Human,Mouse (predicted: Rat,Pig,Cow,Chicken,Dog,Horse) |
| 產(chǎn)品應(yīng)用 | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/Test,ICC/IF=1:100
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 85/87 kDa |
| 檢測分子量 | |
| 細(xì)胞定位 | 細(xì)胞核 細(xì)胞漿 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human IKK alpha/IKK beta around the phosphorylation site of Ser180/Ser181: CT(p-S)FV |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
Nuclear factor kappa B (NFkB) is a ubiquitous transcription factor and an essential mediator of gene expression during activation of immune and inflammatory responses. NFkB 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 NFkB 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 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. 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. SWISS: O15111 Gene ID: 1147 Database links: Entrez Gene: 1147 Human Entrez Gene: 3551 Human Entrez Gene: 12675 Mouse Entrez Gene: 16150 Mouse Omim: 600664 Human Omim: 603258 Human SwissProt: O14920 Human SwissProt: O15111 Human SwissProt: O88351 Mouse SwissProt: Q60680 Mouse Unigene: 198998 Human Unigene: 413513 Human |
| 產(chǎn)品圖片 |
Paraformaldehyde-fixed, paraffin embedded (Mouse small intestine); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (Phospho-IKK alpha(Ser180) + IKK beta(Ser181)) Polyclonal Antibody, Unconjugated (bs-3236R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.
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