纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | MT-ATP6 |
Uniprot No | P00846 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-226 |
氨基酸序列 | MNENLFASFIAPTILGLPAAVLIILFPPLLIPTSKYLINNRLITTQQWLIKLTSKQMMTMHNTKGRTWSLMLVSLIIFIATTNLLGLLPHSFTPTTQLSMNLAMAIPLWAGTVIMGFRSKIKNALAHFLPQGTPTPLIPMLVIIETISLLIQPMALAVRLTANITAGHLLMHLIGSATLAMSTINLPSTLIIFTILILLTILEIAVALIQAYVFTLLVSLYLHDNT |
预测分子量 | 24.8kDa |
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MT-ATP6重组蛋白的3篇参考文献及其摘要概括:
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1. **文献名称**: *Functional analysis of mitochondrial ATP synthase subunit 6 mutations in yeast*
**作者**: Kucharczyk R, et al.
**摘要**: 研究通过酵母模型表达重组人源MT-ATP6蛋白,验证其在线粒体ATP酶复合体组装中的作用,并分析Leber遗传性视神经病变相关突变的致病机制,发现特定突变导致质子通道功能异常。
2. **文献名称**: *Recombinant expression and purification of human mitochondrial ATP synthase subunit 6 in E. coli*
**作者**: Smith J, et al.
**摘要**: 报道了利用大肠杆菌系统成功表达并纯化重组MT-ATP6蛋白,优化了跨膜结构域的溶解条件,为后续结构分析和药物靶点研究提供技术基础。
3. **文献名称**: *Mitochondrial ATP6 mutations alter cellular energy metabolism and oxidative stress response*
**作者**: Garcia-Sanchez A, et al.
**摘要**: 通过哺乳动物细胞系表达突变型MT-ATP6重组蛋白,揭示其导致ATP合成效率下降、活性氧(ROS)水平升高,并引发细胞凋亡,解释了其在神经退行性疾病中的作用。
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注:上述文献为示例,实际研究中建议通过PubMed或Web of Science检索最新论文。若需具体文章,可提供更详细的研究方向(如疾病关联或结构解析)。
**Background of MT-ATP6 Recombinant Protein**
MT-ATP6 is a mitochondrial gene-encoded subunit of ATP synthase (Complex V), a critical enzyme in oxidative phosphorylation (OXPHOS) responsible for generating adenosine triphosphate (ATP), the primary energy currency of cells. This 226-amino acid protein forms part of the FO transmembrane domain of ATP synthase, contributing to proton translocation across the mitochondrial inner membrane, which drives ATP synthesis. Mutations in MT-ATP6 are linked to mitochondrial disorders, such as Leigh syndrome, neuropathy, ataxia, and retinitis pigmentosa (NARP), underscoring its role in cellular energy metabolism.
Recombinant MT-ATP6 protein is produced using heterologous expression systems (e.g., *E. coli* or yeast) to enable detailed biochemical and structural studies. Its production involves cloning the MT-ATP6 gene into expression vectors, followed by protein purification via affinity chromatography. Challenges include ensuring proper folding and membrane integration, as MT-ATP6 is a hydrophobic, multi-pass transmembrane protein.
Research on recombinant MT-ATP6 aids in elucidating mechanisms of ATP synthase dysfunction in mitochondrial diseases, drug screening, and developing gene therapies. It also serves as a tool to study proton transport dynamics, structure-function relationships, and the impact of pathogenic mutations. By providing a controlled source of the protein, recombinant MT-ATP6 facilitates advancements in understanding mitochondrial bioenergetics and therapeutic interventions for energy metabolism disorders.
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