| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CLDN16 |
| Uniprot No | Q9Y5I7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-235aa |
| 氨基酸序列 | MRDLLQYIACFFAFFSAGFLIVATWTDCWMVNADDSLEVSTKCRGLWWECVTNAFDGIRTCDEYDSILAEHPLKLVVTRALMITADILAGFGFLTLLLGLDCVKFLPDEPYIKVRICFVAGATLLIAGTPGIIGSVWYAVDVYVERSTLVLHNIFLGIQYKFGWSCWLGMAGSLGCFLAGAVLTCCLYLFKDVGPERNYPYSLRKAYSAAGVSMAKSYSAPRTETAKMYAVDTRV |
| 预测分子量 | 26 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CLDN16重组蛋白的3篇参考文献示例(注：文献信息为模拟概括，非真实存在)：
1. **"Functional Characterization of Claudin-16 in Renal Tight Junction Formation"**
- 作者：Hou, J.; Konrad, M.
- 摘要：研究通过重组CLDN16蛋白表达，揭示了其在肾脏上皮细胞紧密连接中的核心作用，发现其与CLDN19的协同作用对维持镁离子选择性通透至关重要，突变会导致家族性低镁血症。
2. **"Structural Insights into CLDN16 Recombinant Protein Using Cryo-EM"**
- 作者：Furuse, M.; Tsukita, S.
- 摘要：利用重组CLDN16蛋白进行冷冻电镜结构解析，首次展示了其四跨膜结构域的空间构象，为理解其离子通道功能及致病突变机制提供了分子基础。
3. **"CLDN16 Mutations Disrupt Paracellular Mg²⁺ Transport in a Reconstituted Cell Model"**
- 作者：Weber, S.; et al.
- 摘要：通过体外表达重组CLDN16突变体，证明其功能缺失会破坏细胞单层的镁离子通透性，为FHHNC疾病模型提供了直接实验证据。
(注：若需真实文献，建议通过PubMed或Sci-Hub检索关键词如 "CLDN16 recombinant expression" "CLDN16 structure/function" 获取。)
Claudin-16 (CLDN16) is a key member of the claudin family, a group of transmembrane proteins essential for forming tight junctions in epithelial and endothelial cells. These junctions regulate paracellular permeability, maintaining cellular polarity and selective ion transport. CLDN16 is predominantly expressed in the thick ascending limb of the kidney's loop of Henle, where it plays a critical role in paracellular reabsorption of magnesium (Mg²⁺) and calcium (Ca²⁺). Mutations in the CLDN16 gene are linked to familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), a rare autosomal recessive disorder characterized by severe electrolyte imbalances, kidney stones, and progressive renal failure.
Recombinant CLDN16 protein is engineered using biotechnological platforms (e.g., bacterial, mammalian, or insect cell systems) to produce purified, functional protein for research and therapeutic exploration. Its production typically involves cloning the CLDN16 gene into expression vectors, followed by transfection, protein purification (e.g., affinity chromatography), and validation via Western blot or mass spectrometry. Recombinant CLDN16 enables studies on structure-function relationships, disease mechanisms (e.g., how mutations disrupt tight junction integrity), and drug screening for corrective therapies. It also serves as a potential tool for developing protein replacement strategies or gene therapies targeting FHHNC. However, challenges remain in mimicking its native membrane-bound conformation and post-translational modifications, necessitating optimized expression systems. Current research focuses on leveraging recombinant CLDN16 to design in vitro models of renal transport and to identify modulators that enhance or restore its function in disease contexts.
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