| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATPIF1 |
| Uniprot No | Q9UII2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 26-106aa |
| 氨基酸序列 | GSDQS ENVDRGAGSI REAGGAFGKR EQAEEERYFR AQSREQLAAL KKHHEEEIVH HKKEIERLQK EIERHKQKIK MLKHDD |
| 预测分子量 | 12,2 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ATPIF1重组蛋白的3条文献示例(内容为虚构，仅供格式参考)：
1. **文献名称**：*"Recombinant ATPIF1 regulates mitochondrial ATP synthase activity in hypoxia"*
**作者**：Zhang L, et al.
**摘要**：研究通过大肠杆菌表达系统纯化重组ATPIF1蛋白，发现其在低氧条件下通过抑制ATP合酶活性维持线粒体膜电位，揭示了其在细胞能量稳态中的调控作用。
2. **文献名称**：*"Structural insights into ATPIF1-mediated inhibition of F1Fo-ATPase"*
**作者**：Smith JR, et al.
**摘要**：利用重组ATPIF1蛋白进行X射线晶体学分析，解析其与线粒体ATP合酶的相互作用位点，阐明其通过构象变化抑制酶活性的分子机制。
3. **文献名称**：*"ATPIF1 overexpression exacerbates cardiac ischemia-reperfusion injury via metabolic dysregulation"*
**作者**：Wang Y, et al.
**摘要**：通过重组ATPIF1蛋白在心肌细胞中的功能实验，证明其过度表达会导致ATP合成减少，加剧缺血再灌注损伤，提示其作为潜在治疗靶点。
4. **文献名称**：*"ATPIF1 recombinant protein delivery rescues neuronal viability in mitochondrial dysfunction models"*
**作者**：Garcia M, et al.
**摘要**：开发基于重组ATPIF1的蛋白递送系统，在帕金森病细胞模型中验证其通过调节ATP水解/合成平衡改善神经元存活的能力。
(注：以上文献及作者名为虚构，如需真实文献请通过学术数据库检索关键词“ATPIF1 recombinant”或“ATPase inhibitory factor 1”。)
ATPIF1 (ATPase Inhibitory Factor 1), also known as IF1. is a mitochondrial protein that plays a critical role in regulating ATP synthase activity. Under normal physiological conditions, ATP synthase catalyzes ATP production via oxidative phosphorylation. However, during metabolic stress (e.g., hypoxia or ischemia), when the mitochondrial proton gradient collapses, ATP synthase can reverse its function, hydrolyzing ATP and exacerbating energy depletion. ATPIF1 acts as a natural inhibitor of this reverse activity by binding to ATP synthase, thereby preventing ATP hydrolysis and conserving cellular energy. This pH-dependent interaction is crucial for maintaining energy homeostasis during pathological conditions.
Recombinant ATPIF1 protein is engineered for in vitro studies to dissect its regulatory mechanisms and therapeutic potential. Structurally, human ATPIF1 is a small protein (~10 kDa) containing a mitochondrial targeting sequence and a conserved inhibitory domain. Recombinant versions often exclude the targeting sequence to focus on functional domains. Researchers utilize techniques like bacterial or mammalian expression systems to produce purified ATPIF1. enabling biochemical assays, structural analysis (e.g., X-ray crystallography), and interaction studies with ATP synthase subunits.
Interest in ATPIF1 extends to its implications in diseases such as cancer, neurodegenerative disorders, and metabolic syndromes. Overexpression of ATPIF1 in cancer cells has been linked to chemoresistance by promoting a metabolic shift toward glycolysis, while its downregulation in neurodegeneration may exacerbate energy deficits. Recombinant ATPIF1 serves as a tool to explore these pathways and develop targeted therapies. Additionally, its role in ischemia-reperfusion injury highlights potential applications in cardioprotection.
In summary, recombinant ATPIF1 is vital for advancing our understanding of mitochondrial bioenergetics, disease mechanisms, and therapeutic strategies centered on metabolic regulation.
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