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- 详细信息
- 文献和实验
- 技术资料
- 供应商：
优利科（上海）生命科学有限公司
- 库存：
100
- 靶点：
详询
- 级别：
科研
- 目录编号：
/
- 克隆性：
多克隆
- 抗原来源：
详见说明书
- 保质期：
1年
- 抗体英文名：
Anti-Phospho-IKK alpha/beta (Ser176/Ser180)
- 抗体名：
Phospho-IKK alpha/beta (Ser176/Ser180)抗体
- 标记物：
详询
- 宿主：
兔
- 适应物种：
/
- 免疫原：
见产品详情
- 亚型：
IgG
- 形态：
冻干或液体
- 应用范围：
见产品详情
- 保存条件：
-20℃
- 浓度：
1mg/ml
- 规格：
详询
| 英文名称 Anti-Phospho-IKK alpha/beta (Ser176/Ser180) |
| 中文名称 磷酸化KB抑制蛋白激酶α/β抗体 |
| 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; 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; Conserved Helix Loop Helix Ubiquitous Kinase; Conserved helix loop ubiquitous kinase; I Kappa B Kinase 1; IKKA_HUMAN. |
| I kappa B kinase 2; I kappa B kinase beta; IkBKB; IKK 2; IKK B; IKK beta; IKK2; IKKB; Inhibitor of kappa light chain gene enhancer in B cells; Inhibitor of kappa light polypeptide gene enhancer in B cells; Inhibitor of kappa light polypeptide gene enhancer in B cells kinase beta; Inhibitor of nuclear factor kappa B kinase beta subunit; Inhibitor of nuclear factor kappa B kinase subunit beta; MGC131801; NFKBIKB; Nuclear factor NF kappa B inhibitor kinase beta; Nuclear factor of kappa light chain gene enhancer in B cells inhibitor; IKKB_HUMAN. |
| 浓 度 1mg/1ml |
| 规 格 0.1ml/100μg |
| 抗体来源 Rabbit |
| 克隆类型 polyclonal |
| 交叉反应 Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse |
| 产品类型 一抗 磷酸化抗体 |
研究领域 肿瘤 细胞生物 免疫学 信号转导 转录调节因子 激酶和磷酸酶 细胞粘附分子  |
| 蛋白分子量 predicted molecular weight: 85/87kDa |
| 性 状 Lyophilized or Liquid |
| 免 疫 原 KLH conjugated synthesised phosphopeptide derived from human IKK alpha/beta around the phosphorylation site of Ser176/Ser180 |
| 亚 型 IgG |
| 纯化方法 affinity purified by Protein A |
| 储 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide |
| 产品应用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 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. |
| 保存条件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
产品介绍 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 : IKK beta: Highly expressed in heart, placenta, skeletal muscle, kidney, pancreas, spleen, thymus, prostate, testis and peripheral blood. |
| IKK alpha: 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. |
Database links : UniProtKB/Swiss-Prot: O14920.1 |
| Anti-FGFR2（Fibroblast Growth Factor Receptor 2） 成纤维细胞生长因子受体2抗体 |
| Anti-FGFR3（Fibroblast Growth Factor Receptor 3） 成纤维细胞生长因子受体3抗体 |
| Anti-FGFR4（Fibroblast Growth Factor Receptor 4） 成纤维细胞生长因子受体4抗体 |
| Anti-fgl2 (Fibrinogen-like 2) 凝血酶原酶抗体/纤维介素蛋白/前凝血素抗体 |
| anti-Fibulin 1 抗“衰老关键蛋白”抗体 |
| Anti-Fibulin-5 抗“衰老关键蛋白”抗体 |
| Anti-FLIP S/L （Flice-like Inhibitory Protein） 凋亡调节基因之一抗体 |
| Anti-FLIPS (Flice-like Inhibitory Protein S) 凋亡调节基因之一抗体（短型） |
| Anti-FN (Fibronectin) 纤维连结蛋白抗体 |
| Anti-FOSB FosB抗体 |
| Anti-FOSL1 (FOS-like antigen-1) FOSL1抗体 |
| Anti-FOSL2 (FOS-like antigen-2) FOSL2抗体 |
| anti-FoxP1（Forkhead box P1） FoxP1（T细胞转录因子）抗体 |
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文献和实验相关实验
3 篇 Nature 连发，解决世纪难题，周期蛋白的毁灭调控蕴含癌症患者的新生
在 cyclin D 上，被泛素化标记的 cyclin D 将会被蛋白酶体降解。此外研究还发现，AMBRA1 缺失会导致 cyclin D 和 MYC 蛋白水平升高。cyclin D 与 CDK4/6 结合，使 RB1 蛋白磷酸化。磷酸化 RB1 释放 E2F 转录因子来驱动细胞周期进程所需基因的表达。在 AMBRA1 缺失的细胞中，cyclin D 也能与 CDK2 激酶形成复合物，使癌细胞能够抵抗 CDK4/6 抑制剂的治疗。高水平的 cyclin D 会促进细胞增殖，从而导致 DNA 损伤、复制应激
于JNK，而影响细胞的凋亡。 请各位高手指点一下 您所讲的问题即为在氧化应激的过程中JNK通路的“cross-talk”问题。目前研究的比较多的是有关氧化应激的过程中NF-kb通路通过其靶基因XIAP 和 GADD45对JNK起抑制效应（如图）。此外，还有研究指出，在氧化应激引起的凋亡过程中，MAPKs通路本身的一些激酶（如MKP1，3，5，7）也对JNK起抑制作用。 我知道的很有限，欢迎其他战友补充。
的作用是调控基因表达。例如组蛋白甲基化多导致基因沉默，去甲基化则相反；乙酰化一般是转录激活，去乙酰化则相反。当然，也可在此基础上产生复杂的生物学效应。例如组蛋白去乙酰化酶 HDAC 可影响免疫系统；H3K4me3、H3K9me2 能够调控记忆的形成, 而且 H3K 甲基化与 X 染色体失活、基因组印记和异染色质形成有关；H3 乙酰化通过多种机制调控以来 ATP 的染色质重塑 ，并参与炎症反应；H2A、H2B 泛素化则与 DNA 损害反应有关；而 H3S28 磷酸化与 H3K27 乙酰化可激活转录
磷酸化KB抑制蛋白激酶α/β抗体
￥1680
