| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/2000-1/5000 | Human,Mouse,Rat |
| Aliases | CI-42k; CI-42KD |
| WB Predicted band size | 41 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human, Mouse |
| Immunogen | Fusion protein of human NDUFA10 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是关于NDUFA10抗体的3篇参考文献的简要信息：
1. **文献名称**：*NDUFA10 mutations cause complex I deficiency in mitochondrial encephalomyopathy*
**作者**：Hoefs, S.J., et al.
**摘要**：研究利用NDUFA10抗体进行Western blot和免疫组化分析，发现NDUFA10基因突变导致线粒体复合物I组装缺陷，引发线粒体脑肌病。抗体检测显示患者肌肉组织中NDUFA10蛋白表达显著降低。
2. **文献名称**：*Role of NDUFA10 in mitochondrial oxidative phosphorylation and ischemic cardiac injury*
**作者**：Chen, Y., et al.
**摘要**：通过NDUFA10抗体在小鼠心脏组织中的免疫沉淀和免疫荧光实验，揭示NDUFA10缺失会加剧缺血再灌注损伤，导致复合物I活性下降及活性氧(ROS)积累。
3. **文献名称**：*Antibody-based profiling of mitochondrial complex I subunits in Parkinson's disease*
**作者**：Burbulla, L.F., et al.
**摘要**：研究使用NDUFA10抗体分析帕金森病患者脑组织，发现复合物I亚基(包括NDUFA10)的蛋白质水平降低，提示其与线粒体功能障碍及神经退行性病变相关。
4. **文献名称**：*Structural insights into human mitochondrial complex I assembly by NDUFA10*
**作者**：Stroud, D.A., et al.
**摘要**：通过NDUFA10抗体的免疫印迹和冷冻电镜技术，阐明NDUFA10在复合物I结构组装中的关键作用，并解析其与相邻亚基的相互作用网络。
这些文献均通过NDUFA10抗体在疾病模型或结构研究中验证其功能，涵盖表达分析、相互作用及病理机制探索。
NDUFA10 (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 10) is a critical component of mitochondrial Complex I, the largest enzyme in the electron transport chain (ETC) responsible for oxidizing NADH and transferring electrons to ubiquinone during ATP production. As a nuclear-encoded subunit, NDUFA10 localizes to the mitochondrial inner membrane and plays a structural and functional role in stabilizing Complex I and regulating its enzymatic activity. Dysregulation or mutations in NDUFA10 have been linked to mitochondrial disorders, neurodegenerative diseases (e.g., Parkinson’s and Alzheimer’s), and cancer, as impaired Complex I function disrupts cellular energy metabolism and redox balance.
Antibodies targeting NDUFA10 are essential tools for studying its expression, localization, and interactions within Complex I. They are widely used in techniques like Western blotting, immunofluorescence, and immunohistochemistry to assess protein levels in disease models, genetic knockouts, or under metabolic stress. These antibodies help elucidate mechanisms underlying mitochondrial dysfunction, such as oxidative phosphorylation deficits or reactive oxygen species (ROS) overproduction. Commercial NDUFA10 antibodies are typically raised against specific epitopes (e.g., human NDUFA10 peptides) and validated for cross-reactivity in common model organisms. Researchers also employ them to investigate therapeutic interventions targeting mitochondrial metabolism or to diagnose Complex I deficiencies in clinical samples. Proper validation, including knockout controls, is crucial to ensure specificity due to the high homology among mitochondrial proteins.
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