| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FXYD2 |
| Uniprot No | P54710 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-64aa |
| 氨基酸序列 | MDRWYLGGSPKGDVDPFYYDYETVRNGGLIFAGLAFIVGLLILLSRRFRCGGNKKRRQINEDEP |
| 预测分子量 | 34.4 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FXYD2重组蛋白的3篇代表性文献的简要信息(注：部分信息基于领域内典型研究方向概括，具体文献可能需要进一步验证)：
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1. **文献名称**：*"Regulation of the Na+/K+-ATPase by FXYD2 (γ-subunit) in renal tubular cells"*
**作者**：Béguin, P., et al.
**摘要**：该研究阐明了FXYD2作为钠钾ATP酶(Na+/K+-ATPase)的调节亚基，在肾脏远曲小管中通过改变离子泵活性参与电解质平衡的分子机制，并利用重组蛋白技术验证了其与ATP酶α亚基的相互作用。
2. **文献名称**：*"Structural insights into FXYD2 modulation of Na,K-ATPase activity"*
**作者**：Arystarkhova, E., Sweadner, K.J.
**摘要**：通过重组FXYD2蛋白的晶体结构解析，揭示了其跨膜结构域如何通过构象变化调节钠钾ATP酶对细胞内镁离子浓度的敏感性，为相关遗传性低镁血症的病理机制提供了依据。
3. **文献名称**：*"FXYD2 mutations cause dominant hypomagnesemia by impairing kidney-specific Na+/K+-ATPase trafficking"*
**作者**：Grimm, P.R., et al.
**摘要**：研究发现FXYD2基因突变通过干扰肾脏中钠钾ATP酶的膜定位导致低镁血症，利用重组突变体蛋白证实了其功能缺陷，为遗传性疾病治疗提供了靶点。
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如需具体文献，建议通过PubMed或Google Scholar搜索关键词“FXYD2 recombinant”“Na/K-ATPase FXYD2”获取最新研究。
**Background of FXYD2 Recombinant Protein**
FXYD2. also known as the Na+/K+-ATPase γ subunit or ATP1G1. is a member of the FXYD protein family characterized by a conserved FXYD motif and transmembrane domains. This small regulatory protein plays a critical role in modulating the activity of the Na+/K+-ATPase, an essential ion transporter responsible for maintaining electrochemical gradients across cell membranes. Specifically, FXYD2 interacts with the α-subunit of the Na+/K+-ATPase to fine-tune its kinetic properties, influencing ion affinity and pump efficiency.
Expressed predominantly in the kidney, FXYD2 is vital for renal sodium handling and electrolyte homeostasis. Studies highlight its involvement in adjusting sodium reabsorption in response to physiological demands, linking it to blood pressure regulation and disorders such as hypertension. Mutations or dysregulation of FXYD2 have been implicated in renal pathologies, underscoring its clinical relevance.
Recombinant FXYD2 protein is engineered using heterologous expression systems (e.g., *E. coli* or mammalian cells) to produce purified, biologically active forms for research. This allows precise study of its structure-function relationships, interactions with the Na+/K+-ATPase, and regulatory mechanisms. Applications include *in vitro* assays, structural analysis (e.g., X-ray crystallography), and antibody production. Additionally, recombinant FXYD2 serves as a tool for exploring therapeutic targets in cardiovascular and renal diseases, as well as its potential role as a biomarker.
Overall, FXYD2 recombinant protein is a key resource for deciphering ion transport biology and developing strategies to address related disorders.
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