| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FXYD5 |
| Uniprot No | Q96DB9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 22-145aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSQTLKDTT SSSSADSTIM DIQVPTRAPD AVYTELQPTS PTPTWPADET PQPQTQTQQL EGTDGPLVTD PETHKSTKAA HPTDDTTTLS ERPSPSTDVQ TDPQTLKPSG FHEDDPFFYD EHTLRKR |
| 预测分子量 | 16 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. |
1. **"FXYD5 modulates Na,K-ATPase function and promotes epithelial-mesenchymal transition in cancer"**
- **作者**: Li et al.
- **摘要**: 该研究通过重组FXYD5蛋白实验，揭示了其在调节Na,K-ATP酶活性中的作用，并证明其过表达通过促进上皮-间充质转化(EMT)增强肿瘤细胞迁移和侵袭能力。
2. **"Recombinant FXYD5 regulates membrane potential and cellular metabolism in breast cancer cells"**
- **作者**: Zhang & Thompson
- **摘要**: 利用重组FXYD5蛋白，研究发现其通过改变细胞膜电位和代谢重编程(如增强糖酵解)，促进乳腺癌细胞的生存和耐药性，提示其作为潜在治疗靶点。
3. **"Structural insights into FXYD5 interaction with the sodium pump"**
- **作者**: Lubarski-Gotliv et al.
- **摘要**: 通过重组FXYD5蛋白的体外结合实验及结构分析，揭示了其与钠泵(Na,K-ATP酶)的相互作用机制，表明其通过特定结构域调控离子转运及信号传导功能。
4. **"FXYD5-mediated modulation of cellular osmotic stress response in renal cells"**
- **作者**: Kometiani et al.
- **摘要**: 研究利用重组FXYD5蛋白，发现其在肾细胞中通过稳定钠泵活性，增强细胞对渗透压应激的适应性，可能参与急性肾损伤的病理过程。
以上文献均聚焦于FXYD5重组蛋白的功能研究，涵盖离子通道调控、癌症转移、结构机制及疾病关联等领域。
FXYD5. also known as dysadherin or regulator of ion channel 5 (RIC), is a member of the FXYD protein family characterized by a conserved FXYD motif and single transmembrane domain. These proteins function as auxiliary subunits of Na+/K+-ATPase, modulating ion transport and cellular electrolyte balance. FXYD5 is encoded by the *FXYD5* gene and consists of two α-helical transmembrane segments linked by extracellular and intracellular loops. Its structure enables interaction with the β-subunit of Na+/K+-ATPase, fine-tuning the enzyme’s kinetic properties to regulate sodium and potassium gradients across cell membranes. This regulation impacts critical processes like cell volume homeostasis, signal transduction, and energy metabolism.
Notably, FXYD5 has gained attention for its role in cancer progression. Overexpression of FXYD5 is observed in various malignancies, including colorectal, breast, and pancreatic cancers, where it correlates with metastatic potential and poor prognosis. Dysadherin promotes tumor cell migration, invasion, and epithelial-mesenchymal transition (EMT) by disrupting cell-cell adhesion (e.g., downregulating E-cadherin) and enhancing interactions with the extracellular matrix. Additionally, it may influence signaling pathways such as NF-κB and integrin-mediated cascades, fostering a pro-metastatic microenvironment.
Recombinant FXYD5 protein, produced via bacterial or mammalian expression systems, serves as a tool to study its biochemical interactions and pathophysiological roles. Purified FXYD5 allows in vitro analysis of its binding partners, post-translational modifications, and regulatory effects on Na+/K+-ATPase activity. Researchers also utilize it to screen therapeutic agents targeting FXYD5-driven oncogenic pathways. Despite its established pro-metastatic role, emerging studies suggest context-dependent functions, warranting further exploration of its tissue-specific mechanisms. Understanding FXYD5’s dual roles in ion transport and cancer biology may unveil novel therapeutic strategies for metastatic diseases.
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