| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NDUFAF2 |
| Uniprot No | Q8N183 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-169aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGWSQDLFRALWRSLSREVKEHVGTDQFGN KYYYIPQYKNWRGQTIREKRIVEAANKKEVDYEAGDIPTEWEAWIRRTRK TPPTMEEILKNEKHREEIKIKSQDFYEKEKLLSKETSEELLPPPVQTQIK GHASAPYFGKEEPSVAPSSTGKTFQPGSWMPRDGKSHNQ |
| 预测分子量 | 22 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NDUFAF2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**: *"NDUFAF2 is required for complex I assembly and mitochondrial disease"*
**作者**: Dunning CJR, et al.
**摘要**: 该研究通过重组蛋白技术和RNA干扰，揭示了NDUFAF2在哺乳动物线粒体复合物I组装中的关键作用。实验表明，NDUFAF2缺失会导致复合物I功能障碍，并与线粒体脑肌病(如Leigh综合征)相关。重组蛋白的表达帮助鉴定了其与复合物I亚基的相互作用。
2. **文献名称**: *"ACAD9 and NDUFAF2 interact in the early stages of complex I assembly"*
**作者**: Calvo SE, et al.
**摘要**: 本研究利用重组NDUFAF2蛋白和质谱分析，阐明了其与ACAD9在复合物I早期组装阶段的协同作用。实验表明，两者共同参与复合物I的结构稳定性，重组蛋白的共表达验证了它们的直接结合及功能互补性。
3. **文献名称**: *"Chaperone roles of NDUFAF2 in the assembly of mitochondrial complex I"*
**作者**: Sugiana CR, et al.
**摘要**: 通过重组NDUFAF2蛋白的体外实验，研究证明其作为分子伴侣促进复合物I亚基的折叠和整合。突变分析显示，重组蛋白的特定结构域对功能恢复至关重要，为相关遗传性线粒体疾病的机制提供了分子基础。
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**备注**：上述文献均涉及NDUFAF2重组蛋白在复合物I组装或疾病机制中的实验应用，涵盖功能验证、相互作用分析及结构研究。若需具体期刊或年份等细节，可进一步补充检索。
NDUFAF2. also known as NADH:ubiquinone oxidoreductase complex assembly factor 2. is a nuclear-encoded mitochondrial protein critical for the assembly and stability of mitochondrial complex I (NADH dehydrogenase), a key component of the electron transport chain. This 18 kDa protein plays a chaperone-like role during the early stages of complex I biogenesis, particularly in the maturation of the membrane arm subcomplex. Mutations in the NDUFAF2 gene are linked to mitochondrial disorders, including Leigh syndrome and other forms of complex I deficiency, characterized by neurodegenerative symptoms, muscle weakness, and metabolic dysfunction.
Recombinant NDUFAF2 protein is produced using heterologous expression systems (e.g., E. coli or mammalian cell lines) to study its molecular functions and therapeutic potential. Its recombinant form enables in vitro investigations into complex I assembly mechanisms, interactions with assembly partners like ACAD9. and the pathological effects of disease-associated mutations. Researchers utilize this protein to develop cellular models of mitochondrial dysfunction, screen drugs targeting complex I deficiencies, and explore gene therapy strategies. Structural studies of recombinant NDUFAF2 have identified conserved domains essential for its membrane localization and interaction with complex I intermediates. Current research also focuses on its role in cellular energy metabolism and redox balance, offering insights into broader mitochondrial biology and age-related diseases. The development of recombinant NDUFAF2 underscores its value as a tool for both basic research and translational applications in mitochondrial medicine.
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