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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 (Tyr463)
- 抗体名：
phospho-IKK alpha (Tyr463)抗体
- 标记物：
详询
- 宿主：
详询
- 适应物种：
/
- 免疫原：
见产品详情
- 亚型：
IgG
- 形态：
Lyophilized or Liquid
- 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 (Tyr463) |
| 中文名称 磷酸化KB抑制蛋白激酶α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. |
| 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, Rabbit, Sheep, Guinea Pig |
| 产品类型 一抗 磷酸化抗体 |
研究领域 肿瘤 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: 85kDa |
| 性 状 Lyophilized or Liquid |
| 免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human IKK alpha around the phosphorylation site of Tyr463 |
| 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 : 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 |
| E7 protein/HPV 16 (Human papillomavirus type 16) 人乳头瘤病毒16型E7蛋白抗原 |
| EGF-R （Epidemal growth factor receptor） 表皮生长因子受体（抗原） |
| EGF-R （Epidemal growth factor receptor） 表皮生长因子受体（抗原） |
| Eukaryotic aspartyl protease(Rice) 天冬氨酸蛋白酶家族蛋白(水稻蛋白的一种)（抗原） |
| FAM3B/PANDER(PANcreatic DERived factor) 一种新型的胰岛细胞因子(抗原) |
| Fabp2 (fatty acid binding protein 2, intestinal) 脂肪酸结合蛋白2(抗原) |
| ECG2 (sophagus cancer-related gene-2) 食道癌相关基因（抗原） |
| Fibronectin (FN) 纤维连结蛋白(多肽抗原) |
| FGF-7/KGF （Keratinocyte growth factor precursor) 成纤维细胞生长因子-7/纤维母细胞生长因子 (抗原) |
FGFR(bFGF-R;FGFR-1;FGF receptor-1;c-fgr) 碱性成纤维细胞生长因子受体-1（抗原） |
| HIV gp41 艾滋病病毒（抗原） |
| histone H3-like protein 抗组蛋白H3样抗原 |
| histone H3-like protein 抗组蛋白H3样蛋白（C端抗原） |
| histone H3-like protein 抗组蛋白H3样蛋白（N端抗原） |
| HIV-1（human immunodeficiency virus type 1） 艾滋病病毒-1/人类免疫缺陷病毒1型(抗原) |
| HIV-1（human immunodeficiency virus type 1） 艾滋病病毒-1/人类免疫缺陷病毒1型(抗原) |
| Measles virus protein(Plant2 derived measles virus hemagglutinin protein) 麻疹病毒红血球凝集素蛋白多肽 |
| Measles virus protein(Plant2 derived measles virus hemagglutinin protein) 麻疹病毒红血球凝集素蛋白多肽 |
| HMGB1 (High Mobility Group Box protein 1) 高迁移率族蛋白-1(抗原) |
| HSL(hormone-sensitive lipase) 荷尔蒙敏感脂肪酸（抗原） |
| HSP-27(Heat Shock Protein 27) 热休克蛋白-27(抗原) |
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文献和实验相关实验
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2 从线粒体外膜脱落，进入细胞浆中。在细胞浆中，HK2 结合 NF-κB 的抑制因子 IκBα。 重要的是，HK2 发挥了不依赖于其经典代谢功能的新功能，即作为一个蛋白激酶磷酸化 IκBα 的 Thr 291 位点。该磷酸化促进了蛋白酶 μ-calpain 与 IκBα 的结合并进一步降解 IκBα，进而使转录因子 NF-κB 入核，最终促进了 PD-L1 的表达并导致了肿瘤的免疫逃逸。作者还发现，使用己糖激酶的抑制剂与 PD-1 抗体联用治疗小鼠胶质瘤，可以显著提升 PD-1 抗体的治疗
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。
ws88523758 小弟对于实验处于纯菜鸟，糊里糊涂的做了半年多了，结果数据参差不齐，临近毕业，焦虑万分，特停高手们指导求救！ 我做的是大鼠的系膜细胞，用TNF-α刺激后，再用中药干预24h，测细胞上清中的ikb和NF-KB,用的都是ELISA法。 ikb测值很低，据查当IKBα被磷酸化后分解后，P65和P50才能解离激活。所以，当刺激开始的时候，磷酸化的IKBα上调，IKBα下调。由于P65活化后又可以上调IKBα表达，所以，经过一定时间之后
磷酸化KB抑制蛋白激酶α抗体
￥1680
