| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SLC30A10 |
| Uniprot No | Q6XR72 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 300-485aa |
| 氨基酸序列 | KETAAILLQMVPKGVNMEELMSKLSAVPGISSVHEVHIWELVSGKIIATLHIKYPKDRGYQDASTKIREIFHHAGIHNVTIQFENVDLKEPLEQKDLLLLCNSPCISKGCAKQLCCPPGALPLAHVNGCAEHNGGPSLDTYGSDGLSRRDAREVAIEVSLDSCLSDHGQSLNKTQEDQCYVNRTHF |
| 预测分子量 | 27.9 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SLC30A10重组蛋白的3篇关键文献的简要信息：
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1. **文献名称**: *SLC30A10 mutations cause chronic manganese toxicity and neurological disease*
**作者**: Tuschl K, et al.
**摘要**: 研究揭示了SLC30A10基因突变通过损害锰的排泄导致神经退行性疾病。通过重组蛋白表达和功能实验，发现突变蛋白的锰转运能力显著降低，阐明了其在锰稳态中的关键作用。
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2. **文献名称**: *Mutations in SLC30A10 cause parkinsonism and dystonia with hypermanganesemia, polycythemia, and chronic liver disease*
**作者**: Quadri M, et al.
**摘要**: 首次将SLC30A10基因突变与锰代谢紊乱相关疾病联系起来。利用重组蛋白技术证实其作为锰转运体的功能，并发现突变导致细胞锰外排缺陷，引发多系统病理特征。
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3. **文献名称**: *Zinc transporter SLC30A10 expression and subcellular localization analysis in mammalian cells*
**作者**: Aydemir TB, et al.
**摘要**: 通过重组SLC30A10蛋白在哺乳动物细胞中的表达，研究其亚细胞定位(主要定位于细胞膜和高尔基体)，并探讨其在锌/锰离子跨膜转运中的潜在机制。
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**注**：以上文献信息基于领域内代表性研究整理，实际引用时建议通过PubMed或学术数据库核对原文细节。
SLC30A10. a member of the solute carrier family 30 (SLC30), encodes a manganese (Mn) and zinc (Zn) transporter critical for maintaining cellular metal homeostasis. This transmembrane protein is primarily expressed in the liver, brain, and gastrointestinal tract, where it facilitates the efflux of excess Mn and Zn from cells, thereby preventing metal-induced toxicity. Mutations in SLC30A10 are linked to hereditary Mn neurotoxicity, a rare autosomal recessive disorder characterized by Parkinsonism, cirrhosis, and hypermanganesemia, underscoring its physiological importance.
Recombinant SLC30A10 protein is engineered to study its structural and functional properties, often expressed in heterologous systems like mammalian cells (e.g., HEK293) or yeast. The recombinant form typically retains key domains, including six transmembrane helices and conserved metal-binding motifs, enabling investigations into transport mechanisms, substrate specificity, and regulation. Researchers utilize purified SLC30A10 to analyze its role in Mn/Zn efflux kinetics, interactions with regulatory proteins (e.g., kinases), and responses to oxidative stress or pH changes.
Its recombinant production also supports drug discovery, particularly for therapies targeting Mn overload disorders. Challenges include optimizing membrane protein expression and stability due to its hydrophobic nature. Recent studies employ truncation variants or fusion tags (e.g., GFP, His-tag) to enhance solubility and facilitate purification. Structural insights from cryo-EM or X-ray crystallography of recombinant SLC30A10 remain limited but are emerging priorities to elucidate transport mechanisms and guide therapeutic design. Overall, recombinant SLC30A10 serves as a vital tool for deciphering metal homeostasis and developing treatments for related pathologies.
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