| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NINJ1 |
| Uniprot No | Q92982 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-152aa |
| 氨基酸序列 | MDSGTEEYELNGGLPPGTPGSPDASPARWGWRHGPINVNHYASKKSAAESMLDIALLMANASQLKAVVEQGPSFAFYVPLVVLISISLVLQIGVGVLLIFLVKYDLNNPAKHAKLDFLNNLATGLVFIIVVVNIFITAFGVQKPLMDMAPQQ |
| 预测分子量 | 17.9kDa |
| 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3-4条与NINJ1重组蛋白相关的参考文献示例(部分为假设性概括，实际文献需根据具体研究验证)：
---
1. **文献名称**: *NINJ1 mediates plasma membrane rupture during lytic cell death*
**作者**: Kayagaki, N. et al.
**摘要**: 该研究首次揭示NINJ1蛋白在细胞焦亡过程中介导质膜破裂的机制。通过重组NINJ1蛋白的体外实验，证明其寡聚化可破坏脂质膜完整性，为炎症性疾病治疗提供新靶点。
2. **文献名称**: *Structural basis of NINJ1 assembly in membrane disruption*
**作者**: Yan, Z. et al.
**摘要**: 利用冷冻电镜解析重组人源NINJ1蛋白的寡聚结构，阐明其通过α-螺旋形成跨膜孔道的分子机制，解释了其在细胞程序性死亡中触发膜破裂的功能基础。
3. **文献名称**: *Recombinant NINJ1 promotes neuronal regeneration in a sciatic nerve injury model*
**作者**: Li, X. et al.
**摘要**: 通过原核表达系统制备重组NINJ1蛋白，发现其能激活雪旺细胞迁移信号通路，促进周围神经损伤模型中的轴突再生，提示潜在神经修复应用价值。
4. **文献名称**: *NINJ1 knockout inhibits inflammation by suppressing extracellular vesicle release*
**作者**: Park, S. et al.
**摘要**: 研究采用重组NINJ1蛋白验证其与炎症小体活化关系，发现NINJ1缺失通过减少细胞外囊泡释放降低IL-1β分泌，为抗炎药物开发提供依据。
---
**注**：以上文献为示例性质，具体研究需根据实际发表的论文调整。建议通过PubMed或Web of Science以“NINJ1 recombinant protein”为关键词检索最新成果。
**Background of NINJ1 Recombinant Protein**
NINJ1 (Nerve Injury-Induced Protein 1) is a cell surface protein initially identified for its upregulation following peripheral nerve injury. It belongs to the *ninjurin* family, characterized by two transmembrane domains and a conserved adhesion peptide motif. NINJ1 is expressed in various tissues, including immune cells, neurons, and epithelial cells, and plays roles in cell adhesion, inflammation, and membrane integrity.
Historically, NINJ1 was linked to nerve regeneration and inflammatory responses. However, groundbreaking studies in 2021 revealed its critical function in mediating plasma membrane rupture (PMR) during lytic cell death, such as pyroptosis and necrosis. This discovery positioned NINJ1 as a central executor of cell membrane disruption, a final step in cell death that releases inflammatory signals.
Recombinant NINJ1 protein is produced using expression systems (e.g., *E. coli* or mammalian cells) to enable biochemical and structural studies. Purified NINJ1 facilitates research into its oligomerization, interaction with lipids, and mechanisms underlying PMR. Its recombinant form is also used to develop inhibitors or antibodies targeting pathogenic cell death in conditions like sepsis, neurodegenerative diseases, or autoimmune disorders.
Current research focuses on NINJ1's dual role: while its pro-inflammatory PMR activity exacerbates tissue damage, its adhesion properties may support repair. This duality makes NINJ1 a compelling therapeutic target. Recombinant protein-based tools are vital for dissecting these pathways and advancing drug discovery to modulate NINJ1 in disease contexts.
×
