| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IKBIP |
| Uniprot No | Q70UQ0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-350aa |
| 氨基酸序列 | MSEVKSRKKSGPKGAPAAEPGKRSEGGKTPVARSSGGGGWADPRTCLSLLSLGTCLGLAWFVFQQSEKFAKVENQYQLLKLETNEFQQLQSKISLISEKWQKSEAIMEQLKSFQIIAHLKRLQEEINEVKTWSNRITEKQDILNNSLTTLSQDITKVDQSTTSMAKDVGLKITSVKTDIRRISGLVTDVISLTDSVQELENKIEKVEKNTVKNIGDLLSSSIDRTATLRKTASENSQRINSVKKTLTELKSDFDKHTDRFLSLEGDRAKVLKTVTFANDLKPKVYNLKKDFSRLEPLVNDLTLRIGRLVTDLLQREKEIAFLSEKISNLTIVQAEIKDIKDEIAHISDMN |
| 预测分子量 | 39,3 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IKBIP重组蛋白的3篇参考文献及其摘要概括(基于模拟检索，仅供参考)：
1. **文献名称**：*"Cloning, expression, and functional analysis of recombinant IKBIP in inflammatory signaling"*
**作者**：Zhang Y, Li H, Wang J.
**摘要**：该研究成功构建了IKBIP的重组表达载体，并在HEK293细胞中高效表达纯化。功能实验表明，重组IKBIP通过抑制IKK复合体的活性，负调控NF-κB信号通路，从而减少促炎因子的释放。
2. **文献名称**：*"Structural characterization of IKBIP and its role in cellular stress response"*
**作者**：Chen X, Liu R, Xu M.
**摘要**：通过原核系统表达并纯化IKBIP重组蛋白，利用X射线晶体学解析其三维结构。研究发现，IKBIP通过特定结构域与IKKβ相互作用，并在氧化应激条件下增强细胞存活能力。
3. **文献名称**：*"Recombinant IKBIP modulates autophagy in cancer cells: Implications for therapeutic targeting"*
**作者**：Kim S, Park SM, Lee T.
**摘要**：研究利用哺乳动物表达系统制备重组IKBIP蛋白，发现其过表达可诱导癌细胞自噬，并通过抑制mTOR通路抑制肿瘤生长，提示其在癌症治疗中的潜在应用。
注：以上内容为示例，若需真实文献，建议通过PubMed或Google Scholar以“IKBIP recombinant protein”、“IKKβ interacting protein expression”等关键词检索，并筛选近年发表的研究。
IKBIP (Inhibitor of Kappa B Kinase Interacting Protein) is a regulatory protein involved in modulating the NF-κB signaling pathway, a critical mediator of immune responses, inflammation, and cell survival. Structurally, IKBIP contains a conserved ubiquitin-like domain and interacts with components of the IKK (IκB kinase) complex, particularly IKKγ/NEMO, which is essential for activating NF-κB. By binding to NEMO, IKBIP influences the stability, localization, or activity of the IKK complex, thereby fine-tuning NF-κB activation in response to stimuli like cytokines, pathogens, or stress signals.
Research suggests that IKBIP plays dual roles depending on cellular context. In some settings, it acts as a negative regulator, suppressing excessive NF-κB activation to prevent chronic inflammation or autoimmunity. Conversely, under specific conditions, it may stabilize the IKK complex to promote NF-κB signaling, aiding in cell survival or pathogen defense. Dysregulation of IKBIP has been implicated in diseases such as cancers, inflammatory disorders, and viral infections. For instance, reduced IKBIP expression correlates with enhanced NF-κB activity in certain tumors, potentially driving proliferation and resistance to apoptosis.
Recombinant IKBIP proteins are engineered for functional studies and therapeutic exploration. Produced via bacterial or mammalian expression systems, these proteins retain binding capacity to NEMO and are used to dissect molecular interactions, screen for inhibitors, or develop targeted therapies. Challenges include optimizing solubility and post-translational modifications to mimic native protein behavior. Current research focuses on clarifying IKBIP's regulatory mechanisms and its potential as a biomarker or drug target in NF-κB-related pathologies.
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