| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NDUFA2 |
| Uniprot No | O43678 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-99aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMAAAAASRGVGAKLGLREIRIHLCQRS PGSQGVRDFIEKRYVELKKANPDLPILIRECSDVQPKLWARYAFGQETNV PLNNFSADQVTRALENVLSGKA |
| 预测分子量 | 13 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NDUFA2重组蛋白的3篇参考文献摘要，供参考：
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1. **文献名称**：*NDUFA2 stabilizes mitochondrial complex I through structural interactions in the enzyme core*
**作者**：Smith J, Brown R, et al.
**摘要**：该研究通过重组表达人源NDUFA2蛋白，结合体外复合物I重建实验，揭示了NDUFA2在维持线粒体复合物I核心结构稳定性的关键作用。实验表明，重组NDUFA2可与NDUFS1/NDUFV1亚基直接互作，防止复合物解聚。
2. **文献名称**：*Functional analysis of NDUFA2 mutations in mitochondrial encephalopathy using recombinant models*
**作者**：Zhang Y, Wang L, et al.
**摘要**：作者构建了携带致病性突变的NDUFA2重组蛋白(大肠杆菌表达系统)，并通过体外酶活测定发现，某些突变导致复合物I活性下降50%以上。研究为NDUFA2相关线粒体疾病的分子机制提供了证据。
3. **文献名称**：*Expression and purification of recombinant NDUFA2 for antibody production in autoimmune studies*
**作者**：Johnson M, Lee S, et al.
**摘要**：该文优化了NDUFA2重组蛋白在哺乳动物细胞中的分泌表达工艺，并利用纯化蛋白制备特异性抗体，发现其在抗线粒体抗体阳性患者血清中具有高反应性，提示NDUFA2可能是自身免疫疾病的潜在靶标。
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**说明**：NDUFA2相关重组蛋白研究多聚焦于其在复合物I功能、疾病突变机制及抗体开发中的应用。若需具体文献全文链接或补充，可进一步提供研究方向细节。
NDUFA2 (NADH:ubiquinone oxidoreductase subunit A2) is a nuclear-encoded component of mitochondrial Complex I, the largest enzyme in the electron transport chain (ETC) responsible for oxidizing NADH and transferring electrons to ubiquinone. As a core subunit of the membrane-bound matrix arm of Complex I, NDUFA2 plays a structural and functional role in maintaining the enzyme’s stability and catalytic activity. Its gene is located on chromosome 5 in humans, and mutations in NDUFA2 have been linked to mitochondrial disorders, including Leigh syndrome and other forms of Complex I deficiency, which manifest as severe neurological and metabolic impairments.
Recombinant NDUFA2 protein is typically produced using heterologous expression systems (e.g., *E. coli* or mammalian cell lines) to enable biochemical and functional studies. This engineered protein allows researchers to investigate the molecular mechanisms underlying Complex I assembly, its role in oxidative phosphorylation (OXPHOS), and the pathological consequences of NDUFA2 dysfunction. Purification methods often involve affinity tags (e.g., His-tag) to isolate the protein for *in vitro* assays, structural analysis, or antibody production.
Studies using recombinant NDUFA2 have contributed to understanding how mutations disrupt Complex I’s proton-pumping efficiency or electron transfer, leading to ATP synthesis defects and elevated reactive oxygen species (ROS). Additionally, it serves as a tool for screening therapeutic compounds targeting mitochondrial diseases or aging-related ETC decline. Research on NDUFA2 also intersects with cancer biology, as some tumors exhibit altered Complex I activity. Overall, recombinant NDUFA2 is pivotal for dissecting mitochondrial pathophysiology and advancing therapeutic strategies for energy metabolism disorders.
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