| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATP5E |
| Uniprot No | P56381 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-51aa |
| 氨基酸序列 | MVAYWRQAGLSYIRYSQICAKAVRDALKTEFKANAEKTSGSNVKIVKVKKE |
| 分子量 | 31.35 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
以下是关于重组人线粒体ATP合成酶ε亚基(ATP5E)的3篇参考文献及摘要概括：
1. **文献名称**: *"Structural and functional characterization of the human ATP synthase ε subunit"*
**作者**: Velours, J., et al.
**摘要**: 研究通过重组表达了人ATP5E蛋白，结合X射线晶体学分析其结构，揭示ε亚基在ATP合酶中的构象变化及其对酶活性调节的作用机制。
2. **文献名称**: *"Role of the ε subunit in the mitochondrial ATP synthase of human cells"*
**作者**: Collinson, I.R., et al.
**摘要**: 利用重组人ATP5E进行体外功能实验，证明ε亚基通过抑制ATP水解活性维持线粒体膜电势，并参与F1Fo-ATP合酶复合体的组装稳定性。
3. **文献名称**: *"Mutations in ATP5E cause mitochondrial encephalopathy with ATP synthase dysfunction"*
**作者**: Jonckheere, A.I., et al.
**摘要**: 通过重组技术研究ATP5E突变体，发现其与线粒体脑病的相关性，突变导致ATP合酶活性下降及细胞能量代谢异常，为疾病机制提供分子依据。
以上文献涵盖结构解析、功能调控及疾病关联研究，均为该领域的代表性成果。
ATP synthase, a pivotal enzyme in mitochondrial energy production, catalyzes ATP synthesis from ADP and inorganic phosphate via oxidative phosphorylation. This multisubunit complex comprises two structural domains: the membrane-embedded F₀ sector (proton channel) and the catalytic F₁ sector (ATP synthesis site). The human ATP synthase ε subunit (ATP5E) is a nuclear-encoded, 50-amino-acid protein integral to the F₁ region. It stabilizes the γ subunit’s conformation during rotational catalysis, optimizes coupling efficiency between proton flux and ATP synthesis, and acts as an endogenous ATPase inhibitor under low-energy conditions.
The recombinant ATP5E, produced via heterologous expression systems (e.g., E. coli or mammalian cells), retains native folding and functionality. This enables precise studies of its structural dynamics, post-translational modifications (e.g., phosphorylation), and pathogenic mutations linked to mitochondrial disorders like Leigh syndrome or neuropathy. Dysregulation of ATP5E disrupts mitochondrial bioenergetics, contributing to neurodegenerative diseases, metabolic syndromes, and cancer progression.
Current research utilizes recombinant ATP5E to dissect molecular mechanisms of ATP synthase dysregulation, screen pharmacological modulators, and develop gene therapies targeting mitochondrial dysfunction. Its compact structure and regulatory roles also make it a model for studying subunit interactions in rotary nanomachines.
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