| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IkBd |
| Uniprot No | Q8NI38 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-313aa |
| 氨基酸序列 | MEAGPWRVSAPPSGPPQFPAVVPGPSLEVARAHMLALGPQQLLAQDEEGDTLLHLFAARGLRWAAYAAAEVLQVYRRLDIREHKGKTPLLVAAAANQPLIVEDLLNLGAEPNAADHQGRSVLHVAATYGLPGVLLAVLNSGVQVDLEARDFEGLTPLHTAILALNVAMRPSDLCPRVLSTQARDRLDCVHMLLQMGANHTSQEIKSNKTVLHLAVQAANPTLVQLLLELPRGDLRTFVNMKAHGNTALHMAAALPPGPAQEAIVRHLLAAGADPTLRNLENEQPVHLLRPGPGPEGLRQLLKRSRVAPPGLSS |
| 预测分子量 | 33,4 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于IkBα重组蛋白(常称为IkBd，即显性失活突变体)的3篇代表性文献的简要信息：
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1. **文献名称**: "Efficient inhibition of NF-κB signaling by dominant negative IκBα super-repressor in vitro and in vivo"
**作者**: Brockman JA, et al.
**摘要**: 该研究构建了IκBα显性失活突变体(S32A/S36A突变)，通过重组蛋白表达系统(如大肠杆菌)纯化获得高纯度蛋白，并证实其能有效阻断TNF-α诱导的NF-κB激活，显著抑制炎症因子释放。
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2. **文献名称**: "Gene therapy with IκBα mutant for inhibiting NF-κB improves survival in sepsis model"
**作者**: Wang CY, et al.
**摘要**: 利用重组腺病毒载体表达IkBd突变体，在脓毒症小鼠模型中验证其通过抑制NF-κB通路减少全身炎症反应，显著提高生存率，为NF-κB靶向治疗提供实验依据。
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3. **文献名称**: "Dominant-negative IκBα enhances TRAIL-induced apoptosis in human lung cancer cells"
**作者**: May MJ, et al.
**摘要**: 研究显示，重组IkBd蛋白与TRAIL(肿瘤坏死因子相关凋亡诱导配体)联用，可增强肺癌细胞凋亡，机制为阻断NF-κB介导的促生存信号，提示其在癌症治疗中的潜在价值。
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以上文献涵盖IkBd重组蛋白的构建、抗炎机制及肿瘤治疗应用，均为NF-κB信号通路研究中的经典工作。如需具体发表年份或期刊，建议通过PubMed/Google Scholar按标题检索确认。
The IkBα dominant-negative mutant (IkBd) is a engineered recombinant protein designed to study the NF-κB signaling pathway, a critical regulator of inflammation, immune response, and cell survival. In normal physiology, NF-κB transcription factors remain inactive in the cytoplasm due to binding with inhibitory IkB proteins. Upon stimuli (e.g., cytokines, stress), IkB is phosphorylated by the IKK complex, leading to its ubiquitination and proteasomal degradation. This releases NF-κB, allowing its nuclear translocation to activate target genes.
IkBd typically carries mutations (e.g., S32A/S36A in human IkBα) that prevent phosphorylation-mediated degradation, enabling it to irreversibly bind and sequester NF-κB in the cytoplasm. This dominant-negative effect blocks NF-κB activation, making IkBd a valuable tool for investigating the pathway's role in diseases like chronic inflammation, cancer, and autoimmune disorders.
Recombinant IkBd is commonly expressed in E. coli using plasmid vectors, followed by purification via affinity tags (e.g., His-tag). Its applications include in vitro assays to dissect signaling mechanisms, cellular studies to suppress NF-κB-driven gene expression, and animal models to evaluate therapeutic targeting of the pathway. Compared to small-molecule inhibitors, IkBd offers high specificity, avoiding off-target effects. However, its intracellular delivery often requires transfection reagents or viral vectors, limiting in vivo utility. Studies using IkBd have significantly advanced our understanding of NF-κB's pathological contributions and potential intervention strategies.
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