| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | OPA3 |
| Uniprot No | Q9H6K4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-179aa |
| 氨基酸序列 | MVVGAFPMAKLLYLGIRQVSKPLANRIKEAARRSEFFKTYICLPPAQLYH WVEMRTKMRIMGFRGTVIKPLNEEAAAELGAELLGEATIFIVGGGCLVLE YWRHQAQQRHKEEEQRAAWNALRDEVGHLALALEALQAQVQAAPPQGALE ELRTELQEVRAQLCNPGRSASHAVPASKK |
| 预测分子量 | 19,9 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OPA3重组蛋白的虚构参考文献示例(实际文献请通过学术数据库检索)：
1. **文献名称**：*Structural and Functional Analysis of the OPA3 Protein in Mitochondrial Dynamics*
**作者**：Smith J. et al.
**摘要**：本研究通过重组表达人源OPA3蛋白，结合X射线晶体学解析其三维结构，揭示了OPA3与线粒体膜结合的机制，并发现其突变体导致线粒体分裂异常，提示其在遗传性视神经萎缩中的作用。
2. **文献名称**：*OPA3 Recombinant Protein Rescues Mitochondrial Dysfunction in Cellular Models*
**作者**：Li Y. et al.
**摘要**：构建OPA3重组蛋白表达系统，证明其在OPA3缺陷细胞中恢复线粒体膜电位和ATP生成能力，为基因治疗提供了实验依据。
3. **文献名称**：*Expression and Characterization of OPA3 Mutants Associated with Costeff Syndrome*
**作者**：Garcia R. et al.
**摘要**：通过原核系统表达OPA3常见致病突变体(如p.Q105E)，发现突变导致蛋白稳定性下降及线粒体自噬通路激活异常，解释了Costeff综合征的分子机制。
4. **文献名称**：*OPA3 Recombinant Protein Interacts with Cardiolipin in Mitochondrial Membranes*
**作者**：Wang H. et al.
**摘要**：利用重组OPA3蛋白进行脂质结合实验，发现其特异性结合心磷脂，提示其在线粒体内膜形态维持中的关键作用。
**注意**：以上为模拟文献，实际研究需查阅PubMed、Web of Science等平台，检索关键词如“OPA3 recombinant protein”“OPA3 mitochondrial function”等。
**Background of OPA3 Recombinant Protein**
The OPA3 gene encodes a mitochondrial protein implicated in cellular dynamics, particularly in membrane integrity, mitochondrial morphology, and apoptosis regulation. First linked to human disease through its association with autosomal dominant optic atrophy type 3 (ADOA3) and Costeff syndrome (a rare autosomal recessive disorder), OPA3 mutations disrupt mitochondrial function, leading to neurodegeneration, vision loss, and metabolic abnormalities. The OPA3 protein is ubiquitously expressed but highly enriched in tissues with high metabolic demands, such as the brain and retina, underscoring its role in energy homeostasis.
Structurally, OPA3 contains a conserved mitochondrial targeting sequence and a putative transmembrane domain, suggesting localization to mitochondrial membranes. While its exact molecular mechanisms remain under investigation, OPA3 is hypothesized to interact with lipid bilayers or proteins involved in mitochondrial fusion-fission dynamics, apoptosis, and reactive oxygen species (ROS) modulation. Dysfunctional OPA3 disrupts these processes, contributing to mitochondrial fragmentation, impaired oxidative phosphorylation, and neuronal degeneration.
Recombinant OPA3 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), enables *in vitro* studies to dissect its biochemical properties and interactions. This tool has been pivotal in characterizing post-translational modifications, binding partners, and functional domains. Additionally, recombinant OPA3 aids in modeling disease mechanisms, screening therapeutic compounds, and developing gene-editing or protein-replacement strategies for OPA3-related disorders.
Research on OPA3 recombinant protein not only advances understanding of mitochondrial biology but also bridges gaps in therapeutic development for neurodegenerative and metabolic diseases linked to mitochondrial dysfunction. Its study highlights the interplay between mitochondrial dynamics and cellular health, offering insights into broader pathologies like Parkinson’s disease and Leigh syndrome.
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