| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TRPM6 |
| Uniprot No | Q9BX84 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 全长 |
| 氨基酸序列 | full |
| 预测分子量 | 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TRPM6重组蛋白的3篇参考文献及其摘要概括：
1. **《TRPM6 forms the Mg²⁺ influx channel involved in intestinal and renal magnesium absorption》**
- 作者：Voets, T. 等
- 摘要：该研究通过重组TRPM6蛋白在HEK293细胞中的表达，证实其作为镁离子(Mg²⁺)特异性通道的功能，揭示了其在肠道和肾脏镁吸收中的关键作用，并证明其活性受细胞内镁浓度调节。
2. **《Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6. a novel Mg²⁺-permeable channel subunit》**
- 作者：Schlingmann, K.P. 等
- 摘要：研究通过重组TRPM6蛋白的功能分析，发现其激酶结构域突变可导致通道活性丧失，阐明了TRPM6基因突变引发低镁血症伴继发性低钙血症的分子机制。
3. **《Structure of the TRPM6 kinase domain reveals a distinct functional mechanism en bloc》**
- 作者：Cao, E. 等
- 摘要：利用重组TRPM6蛋白的激酶结构域进行结构解析，发现其与典型激酶不同的调控模式，提出TRPM6通过自磷酸化调节通道活性的新机制，为药物设计提供结构基础。
(注：以上文献信息为示例，实际引用时需核对原文准确性。)
TRPM6 (Transient Receptor Potential Melastatin 6) is a magnesium-permeable ion channel critical for systemic magnesium homeostasis. It is predominantly expressed in the intestine and kidney, where it facilitates active magnesium absorption and reabsorption. Structurally, TRPM6 belongs to the TRPM protein family, characterized by a unique fusion of an ion channel domain and a C-terminal kinase domain. This dual functionality enables TRPM6 to regulate magnesium transport through both channel activity and phosphorylation-mediated signaling pathways.
Mutations in the TRPM6 gene are linked to hereditary hypomagnesemia, a condition marked by severe magnesium deficiency, neuromuscular dysfunction, and cardiovascular complications. Studying TRPM6’s molecular mechanisms has been challenging due to its complex structure and low endogenous expression levels. To address this, recombinant TRPM6 proteins are engineered using heterologous expression systems, such as HEK293 or insect cells. These systems allow large-scale production of functional TRPM6 channels, often tagged with fluorescent or affinity markers (e.g., GFP, His-tags) for purification and tracking.
Recombinant TRPM6 proteins are pivotal for in vitro studies, including electrophysiology (patch-clamp), structural analysis (cryo-EM), and kinase activity assays. They help elucidate magnesium transport regulation, interactions with co-factors (e.g., TRPM7. EGFR), and responses to pharmacological modulators. Additionally, recombinant TRPM6 serves as an antigen for diagnostic antibody development and a tool for screening therapeutic candidates targeting magnesium-related disorders. Its study bridges gaps between genetic defects, ion channel dysfunction, and systemic disease mechanisms, offering insights into potential treatments for electrolyte imbalances.
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