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核因子κ叠抑制蛋白α抗体

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产物名称: 核因子κ叠抑制蛋白α抗体
产物型号: IKB alpha
产物展商: 单克隆抗体/多克隆抗体
产物文档: 无相关文档

简单介绍

核因子κ叠抑制蛋白α抗体应用于IHC、WB、 IF、IP、ELISA等科研实验,按理化性质和生物学功能IgM、IgG、IgA、IgE、IgD五类。按抗体的来源,可将其分为天然抗体和**抗体。核因子κ叠抑制蛋白α抗体生产每个流程都执行严格的检测标准,保证蛋白抗原产物质量,质量稳定,实验效果明显。


核因子κ叠抑制蛋白α抗体  的详细介绍

核因子κ叠抑制蛋白α抗体

规格:1尘驳/1尘濒

英文名: IKB alpha

别名: NFKBIA; Inhibitor of KB alpha; I kappa B alpha; I(Kappa)B(alpha); IkappaBalpha; IKBA; IKBalpha; MAD 3; MAD3; Major histocompatibility complex enhancer binding protein MAD3; NF kappa B inhibitor alpha;

分子量: 36kDa

储存液:0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce

克隆类型:笔辞濒测肠濒辞苍补濒

亚型:滨驳骋

纯化方法:affinity purified by Protein A

**原:KLH conjugated synthetic peptide derived from human IKB alph

交叉反应:Human, Mouse, Rat,

细胞定位:细胞核 细胞浆

核因子κ叠抑制蛋白α抗体产物介绍:background: Three major forms of IKB like molecules have been identified and each is characterised by multiple copies of ankyrin repeats. IKB alpha and IKB beta appear to be the major regulatory forms of IKB in most cells. These proteins interact with p65 or cRel containing forms of NFkB and block nuclear import by masking the nuclear localisation sequences of NFkB. The activation of NFkB involves the inducible phosphorylation and subsequent degradation of IKB. Immunoblotting easily detects the hyperphosphorylated forms of IKB alpha, but not phosphorylated IKB beta. Interestingly, IKB alpha and IKB beta mediate different NFkB responses. IkB alpha appears to control more transient activation of NFkB in response to an inducer, while IKB beta controls a persistent response. Bcl3 interacts with p50 and p52 containing forms of NFkB, but rather than being an inhibitor it appears to function to stimulate transcription. The degradation of IKB is confirmed by immunoblotting. Function: Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription. Subunit: Interacts with RELA; the interaction requires the nuclear import signal核因子κ叠抑制蛋白α抗体. Interacts with NKIRAS1 and NKIRAS2. Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, IKBKAP and MAP3K14. Interacts with HBV protein X. Interacts with RWDD3; the interaction enhances sumoylation. Interacts (when phosphorylated at the 2 serine residues in the destruction motif D-S-G-X(2,3,4)-S) with BTRC. Associates with the SCF(BTRC) complex, composed of SKP1, CUL1 and BTRC; the association is mediated via interaction with BTRC. Part of a SCF(BTRC)-like complex lacking CUL1, which is associated with RELA; RELA interacts directly with NFKBIA. Interacts with PRMT2. Interacts with PRKACA in platelets; this interaction is disrupted by thrombin and collagen. Interacts with HIF1AN. Subcellular Location: Cytoplasm. Nucleus. Tissue Specificity: Highly expressed in lymph node, thymus followed by liver, brain, muscle, kidney, gastrointestinal and reproductive tract. Post-translational modifications: Phosphorylated; disables inhibition of NF-kappa-B DNA-binding activity. Phosphorylation 核因子κ叠抑制蛋白α抗体at positions 32 and 36 is prerequisite to recognition by UBE2D3 leading to polyubiquitination and subsequent degradation. Sumoylated; sumoylation requires the presence of the nuclear import signal. Monoubiquitinated at Lys-21 and/or Lys-22 by UBE2D3. Ubiquitin chain elongation is then performed by CDC34 in cooperation with the SCF(FBXW11) E3 ligase complex, building ubiquitin chains from the UBE2D3-primed NFKBIA-linked ubiquitin. The resulting polyubiquitination leads to protein degradation. Also ubiquitinated by SCF(BTRC) following stimulus-dependent phosphorylation at Ser-32 and Ser-36. Deubiquitinated by porcine reproductive and respiratory syndrome virus Nsp2 protein, which thereby interferes with NFKBIA degradation and impairs subsequent NF-kappa-B activation. DISEASE: Defects in NFKBIA are the cause of ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant (ADEDAID) [MIM:612132]. Ectodermal dysplasia defines a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. ADEDAID is an ectodermal dysplasia associated with decreased production of pro-inflammatory cytokines and certain interferons, rendering patients susceptible to infection. Similarity: Belongs to the NF-kappa-B inhibitor family. Contains 5 ANK repeats. Gene ID: 4792 Database links: Entrez Gene: 4792 Human Entrez Gene: 18035 Mouse Entrez Gene: 25493 Rat Omim: 164008 Human SwissProt: P25963 Human SwissProt: Q9Z1E3 Mouse SwissProt: Q63746 Rat Unigene: 81328 Human Unigene: 170515 Mouse Unigene: 12550 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 转录调节因子(Transcriptin Regulators)

核因子κ叠抑制蛋白α抗体产物应用:WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1:50-300 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  转录调节因子  激酶和磷酸酶  

储存条件: Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.

来源: Rabbit

外观: Lyophilized or Liquid


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