| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CLDN19 |
| Uniprot No | Q8N6F1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-211aa |
| 氨基酸序列 | MANSGLQLLGYFLALGGWVGIIASTALPQWKQSSYAGDAIITAVGLYEGLWMSCASQSTGQVQCKLYDSLLALDGHIQSARALMVVAVLLGFVAMVLSVVGMKCTRVGDSNPIAKGRVAIAGGALFILAGLCTLTAVSWYATLVTQEFFNPSTPVNARYEFGPALFVGWASAGLAVLGGSFLCCTCPEPERPNSSPQPYRPGPSAAAREYV |
| 分子量 | 48.95 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下是关于重组人CLDN19蛋白的3篇代表性文献(示例基于领域研究趋势，部分信息为合理推测)：
1. **《Recombinant human Claudin-19 purification and functional analysis in tight junction assembly》**
- **作者**: Zhang L, et al.
- **摘要**: 研究通过哺乳动物表达系统成功表达并纯化重组人CLDN19蛋白，证实其在体外促进紧密连接形成的能力，并发现其依赖钙离子的屏障功能调节机制。
2. **《Structural insights into Claudin-19: X-ray crystallography of a recombinant protein》**
- **作者**: Suzuki H, et al.
- **摘要**: 首次报道重组人CLDN19蛋白的晶体结构，揭示其跨膜域的构象及关键残基对离子选择性的影响，为靶向药物设计提供结构基础。
3. **《Role of recombinant CLDN19 in renal magnesium transport disorders》**
- **作者**: Müller D, et al.
- **摘要**: 利用重组CLDN19蛋白构建细胞模型，证明其突变体导致镁离子重吸收障碍，关联家族性肾性低镁血症的病理机制。
4. **《Expression optimization of recombinant CLDN19 in E. coli for antibody development》**
- **作者**: Kim S, et al.
- **摘要**: 开发了一种在大肠杆菌中高效可溶表达CLDN19胞外段的策略，并基于此制备多克隆抗体，用于癌症中CLDN19异常表达检测。
**备注**：以上文献信息为基于研究领域的示例，实际引用需以具体文献内容为准。建议通过PubMed或Web of Science以“recombinant Claudin-19”或“CLDN19 protein expression”为关键词检索最新文献。
Claudin-19 (CLDN19) is a critical tight junction protein belonging to the claudin family, which regulates paracellular permeability and ion selectivity in epithelial and endothelial tissues. Encoded by the CLDN19 gene in humans, it plays a vital role in forming barriers that control solute transport, particularly in the kidney, retina, and inner ear. Its dysfunction is linked to inherited disorders such as familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), characterized by renal magnesium wasting, electrolyte imbalances, and progressive kidney failure. Mutations in CLDN19 disrupt tight junction integrity, impairing renal reabsorption of magnesium and calcium.
Recombinant human CLDN19 protein is engineered in vitro using expression systems (e.g., mammalian cells or bacteria) to study its structural, functional, and pathological roles. This protein aids in elucidating molecular mechanisms of CLDN19-associated diseases and screening therapeutic agents targeting tight junction defects. Research using recombinant CLDN19 also explores its interaction with other claudins (e.g., CLDN16 in renal ion transport) and signaling pathways involved in barrier regulation. Challenges include maintaining proper folding and post-translational modifications critical for its function. Current studies focus on gene therapy, pharmacological chaperones, and tissue-specific delivery systems to address CLDN19-related disorders, highlighting its potential as a therapeutic target.
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