| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TIMM17A |
| Uniprot No | Q99595 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-171aa |
| 氨基酸序列 | MEEYAREPCPWRIVDDCGGAFTMGTIGGGIFQAIKGFRNSPVGVNHRLRGSLTAIKTRAPQLGGSFAVWGGLFSMIDCSMVQVRGKEDPWNSITSGALTGAILAARNGPVAMVGSAAMGGILLALIEGAGILLTRFASAQFPNGPQFAEDPSQLPSTQLPSSPFGDYRQYQ |
| 预测分子量 | 45.0 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TIMM17A重组蛋白的虚构参考文献示例(实际文献需通过学术数据库检索)：
---
1. **文献名称**: *Functional characterization of recombinant TIMM17A in mitochondrial protein import*
**作者**: Müller, J., et al.
**摘要**: 本研究通过大肠杆菌表达系统成功纯化重组TIMM17A蛋白，并证明其与TIM23复合体其他亚基的相互作用，揭示其在介导线粒体前体蛋白跨膜转运中的关键作用。实验显示TIMM17A缺失导致线粒体膜电位下降及蛋白导入效率降低。
2. **文献名称**: *Structural insights into TIMM17A regulation by phosphorylation using recombinant protein analysis*
**作者**: Chen, L., & Smith, R.
**摘要**: 利用重组TIMM17A进行体外磷酸化实验，发现酪氨酸激酶修饰可调节其与伴侣蛋白HSP70的结合能力。晶体结构解析显示磷酸化位点位于跨膜结构域附近，影响通道构象及底物识别。
3. **文献名称**: *TIMM17A overexpression in cancer cells: Recombinant protein-based mechanistic study*
**作者**: Tanaka, K., et al.
**摘要**: 通过哺乳动物细胞表达重组TIMM17A，发现其过表达增强肿瘤细胞线粒体代谢活性，并抵抗凋亡。蛋白质组学分析表明，TIMM17A通过调控Bcl-2家族蛋白稳定性促进细胞存活。
---
**建议**：访问PubMed或Google Scholar，使用关键词“TIMM17A recombinant protein”、“TIMM17A purification”或“TIMM17A structure”检索真实文献。
**Background of TIMM17A Recombinant Protein**
TIMM17A (Translocase of Inner Mitochondrial Membrane 17 Homolog A) is a critical component of the mitochondrial TIM23 complex, which mediates the import of nuclear-encoded proteins into the mitochondrial matrix. As an integral membrane protein, TIMM17A anchors the TIM23 translocase to the inner mitochondrial membrane, facilitating the recognition and translocation of precursor proteins with N-terminal targeting signals. Its function is essential for maintaining mitochondrial homeostasis, energy production, and cellular viability, given the reliance of mitochondria on imported proteins for oxidative phosphorylation and metabolic regulation.
The TIMM17A gene is evolutionarily conserved, highlighting its fundamental role in eukaryotic cells. Dysregulation or mutations in TIMM17A have been linked to mitochondrial disorders, neurodegenerative diseases, and cancer, underscoring its biomedical relevance. For instance, impaired TIM23 activity due to TIMM17A deficiency can disrupt mitochondrial proteostasis, leading to bioenergetic failure and apoptosis.
Recombinant TIMM17A protein is generated through heterologous expression systems (e.g., *E. coli* or mammalian cell cultures*) to study its structural and functional properties *in vitro*. This engineered protein retains key domains, including its transmembrane segments and matrix-loop regions, enabling researchers to investigate its interactions with TIM23 partners, substrate proteins, or potential pharmacological modulators.
Applications of recombinant TIMM17A span mechanistic studies of protein import, drug screening for mitochondrial diseases, and exploring its role in pathological contexts like ischemia-reperfusion injury or cancer metabolism. Its availability also aids in developing antibodies or biosensors for diagnostic or therapeutic purposes. Overall, TIMM17A recombinant protein serves as a vital tool for dissecting mitochondrial biology and advancing translational research in mitochondrial medicine.
×
