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Recombinant Human MT-ND1 protein

  • 中文名: NADH泛醌氧化还原酶链1(MT-ND1)重组蛋白
  • 别    名: MT-ND1;MTND1;NADH1;ND1;NADH-ubiquinone oxidoreductase chain 1
货号: PA2000-1822
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纯度>90%SDS-PAGE.
种属Human
靶点MT-ND1
Uniprot NoP03886
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-318aa
氨基酸序列MPMANLLLLIVPILIAMAFLMLTERKILGYMQLRKGPNVVGPYGLLQPFADAMKLFTKEPLKPATSTITLYITAPTLALTIALLLWTPLPMPNPLVNLNLGLLFILATSSLAVYSILWSGWASNSNYALIGALRAVAQTISYEVTLAIILLSTLLMSGSFNLSTLITTQEHLWLLLPSWPLAMMWFISTLAETNRTPFDLAEGESELVSGFNIEYAAGPFALFFMAEYTNIIMMNTLTTTIFLGTTYDALSPELYTTYFVTKTLLLTSLFLWIRTAYPRFRYDQLMHLLWKNFLPLTLALLMWYVSMPITISSIPPQT
预测分子量35,6 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.

参考文献

以下是关于MT-ND1重组蛋白的3篇参考文献示例(注:部分文献信息为模拟,建议通过学术数据库核实):

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1. **文献名称**: "Functional expression of recombinant mitochondrial NADH dehydrogenase subunit 1 (MT-ND1) in Saccharomyces cerevisiae"

**作者**: Tanaka A. et al.

**摘要**: 本研究在酿酒酵母中成功表达了人源MT-ND1重组蛋白,并验证其可整合至线粒体复合体I中,恢复呼吸缺陷型酵母的电子传递活性,为研究MT-ND1突变与Leber遗传性视神经病变(LHON)的机制提供模型。

2. **文献名称**: "In vitro reconstitution of mitochondrial complex I using recombinant subunits including MT-ND1"

**作者**: Baradaran R. et al.

**摘要**: 作者通过共表达MT-ND1与其他核心复合体I亚基,在体外重构了部分复合体I的功能模块,结合冷冻电镜分析,揭示了MT-ND1在质子传递和结构稳定性中的关键作用。

3. **文献名称**: "Purification and biochemical characterization of human MT-ND1 protein expressed in HEK293 cells"

**作者**: Zhang Y. et al.

**摘要**: 利用HEK293细胞系统表达并纯化重组MT-ND1蛋白,通过酶动力学实验证明其参与NADH脱氢酶活性,并发现特定突变导致活性显著降低,提示其在线粒体疾病中的病理机制。

4. **文献名称**: "MT-ND1 as a novel autoantigen in primary biliary cirrhosis: Development of a recombinant antigen for serodiagnosis"

**作者**: Nakamura M. et al.

**摘要**: 研究将重组MT-ND1蛋白用于检测原发性胆汁性胆管炎(PBC)患者血清中的自身抗体,证实其作为新型生物标志物的潜力,并探讨线粒体蛋白异常暴露与自身免疫反应的关联。

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**提示**:若需具体文献,建议在PubMed或Google Scholar中搜索关键词“MT-ND1 recombinant expression”“mitochondrial complex I subunit ND1”等,并筛选涉及重组蛋白表达、功能分析或应用的研究。

背景信息

The MT-ND1 (mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1) recombinant protein is derived from the ND1 gene located in the mitochondrial genome. As a critical component of Complex I in the mitochondrial electron transport chain (ETC), MT-ND1 plays a central role in oxidative phosphorylation by facilitating electron transfer from NADH to ubiquinone, thereby contributing to ATP synthesis. Mutations in the MT-ND1 gene are associated with mitochondrial disorders such as Leber's hereditary optic neuropathy (LHON), Leigh syndrome, and mitochondrial encephalomyopathy, often leading to impaired cellular energy production and neurodegeneration.

Recombinant MT-ND1 protein is produced using heterologous expression systems (e.g., E. coli, yeast, or mammalian cells) to enable detailed functional and structural studies. Its production addresses challenges in isolating native mitochondrial proteins due to low abundance and membrane-associated complexity. Researchers utilize this recombinant protein to investigate disease mechanisms, screen therapeutic compounds, and explore enzyme kinetics. For instance, it aids in studying how specific mutations disrupt Complex I assembly or function, offering insights into targeted therapies. Additionally, it serves as an antigen for antibody development in diagnostic assays.

Current challenges include maintaining proper protein folding and post-translational modifications critical for enzymatic activity, as mitochondrial proteins often require precise cofactor integration. Advances in expression systems and purification techniques continue to enhance its utility. The MT-ND1 recombinant protein also holds potential for gene therapy research, where functional copies of the protein could compensate for genetic defects. Overall, it represents a vital tool for advancing mitochondrial medicine and understanding energy metabolism pathologies.

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