| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PIK3IP1 |
| Uniprot No | Q96FE7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 22-168aa |
| 氨基酸序列 | SGGCFWDNGHLYREDQTSPAPGLRCLNWLDAQSGLASAPVSGAGNHSYCR NPDEDPRGPWCYVSGEAGVPEKRPCEDLRCPETTSQALPAFTTEIQEASE GPGADEVQVFAPANALPARSEAAAVQPVIGISQRVRMNSKEKKDLGTVDH HHHHH |
| 预测分子量 | 17 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PIK3IP1重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**：*PIK3IP1. a negative regulator of PI3K, suppresses inflammation and metabolic dysfunction in mice*
**作者**：He et al.
**摘要内容**：本研究通过构建重组PIK3IP1蛋白，验证其在PI3K/AKT信号通路中的抑制作用。实验表明，重组PIK3IP1通过结合PI3K的p85调节亚基，抑制巨噬细胞中炎症因子的释放，并在高脂饮食小鼠模型中改善胰岛素抵抗和肝脏脂肪变性。
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2. **文献名称**：*Structural and functional characterization of recombinant PIK3IP1 reveals its role in modulating T-cell activation*
**作者**：Wang et al.
**摘要内容**：作者利用大肠杆菌表达系统纯化重组PIK3IP1蛋白，并通过X射线晶体学解析其结构。功能实验显示，该蛋白通过抑制PI3K活性减少CD4+ T细胞的增殖和IL-2分泌，提示其在自身免疫疾病中的潜在治疗价值。
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3. **文献名称**：*Recombinant PIK3IP1 attenuates tumor progression by inhibiting the PI3K pathway in hepatocellular carcinoma*
**作者**：Li et al.
**摘要内容**：研究团队在肝癌细胞系及小鼠移植瘤模型中验证了重组PIK3IP1的抗肿瘤作用。实验表明，该蛋白通过阻断PI3K/mTOR通路抑制肿瘤细胞增殖和血管生成，并增强化疗药物敏感性。
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这些研究聚焦于PIK3IP1重组蛋白的表达、结构解析及其在炎症、代谢疾病和癌症中的调控机制。如需具体文献来源，建议通过PubMed或Google Scholar检索标题及作者获取全文。
PIK3IP1 (Phosphoinositide-3-Kinase Interacting Protein 1) is a regulatory protein that modulates the phosphoinositide-3-kinase (PI3K) signaling pathway, a critical cascade involved in cell growth, survival, metabolism, and immune responses. As a transmembrane protein, PIK3IP1 contains an intracellular pseudokinase domain and an extracellular region, enabling interactions with PI3K components. It functions as a physiological suppressor of PI3K activity by competitively binding to the p110 catalytic subunit of PI3K, thereby inhibiting its interaction with regulatory subunits (e.g., p85) and downstream signaling. This negative regulation helps maintain cellular homeostasis, and its dysregulation has been linked to pathologies such as cancer, autoimmune disorders, and metabolic diseases.
The PI3K pathway is frequently hyperactivated in cancers, driving uncontrolled proliferation and therapy resistance. PIK3IP1 expression is often downregulated in tumors, suggesting its role as a tumor suppressor. Conversely, in autoimmune conditions, impaired PIK3IP1 function may exacerbate inflammation due to unchecked PI3K signaling. Recombinant PIK3IP1 protein, produced via expression systems like *E. coli* or mammalian cells, retains the functional domains necessary for PI3K interaction. It is widely used in mechanistic studies to dissect PI3K regulation, screen for therapeutic agents, or explore its therapeutic potential in restoring pathway balance.
Research on recombinant PIK3IP1 also extends to immunotherapy, as PI3K signaling shapes T-cell activation and tolerance. By modulating this pathway, PIK3IP1 may influence immune cell function, offering avenues for treating immune-related diseases. Its recombinant form serves as a tool to validate binding partners, structure-function relationships, and preclinical efficacy. Overall, PIK3IP1 recombinant protein is a valuable reagent for understanding PI3K biology and developing targeted therapies against PI3K-driven disorders.
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