| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATP5S |
| Uniprot No | Q99766 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-127aa |
| 氨基酸序列 | MCCAVSEQRLTCADQMMLFGKISQQLCGVKKLPWSCDSRYFWGWLNAVFNKVDYDRIRDVGPDRAASEWLLRCGAMVRYHGQERWQKDYNHLPTGPLDKYKIQAIDATDSCIMSIGFDHMETSNICC |
| 分子量 | 39.71 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
1. **"Structural insights into the ATP synthase dimer and its role in mitochondrial cristae formation" by He, J. et al.**
摘要：该研究通过冷冻电镜解析了ATP合酶二聚体结构，揭示了ATP5S亚基在维持二聚体稳定性及线粒体嵴形态形成中的关键作用。
2. **"ATP5S regulates metabolic reprogramming in cancer cells via modulating mitochondrial respiratory chain supercomplexes" by Chen, L. et al.**
摘要：研究发现ATP5S通过调控呼吸链超复合体组装，影响肿瘤细胞能量代谢重编程，其表达缺失导致氧化磷酸化效率下降并促进糖酵解依赖。
3. **"A novel mutation in ATP5S causes mitochondrial encephalopathy with impaired ATP synthase function" by Chen, Y. et al.**
摘要：报道了一种ATP5S基因突变导致线粒体脑病的病例，突变导致ATP合酶活性降低及神经元能量代谢缺陷，证实ATP5S在神经功能中的必要性。
4. **"ATP synthase subunit s interacts with cyclophilin D to mediate mitochondrial permeability transition" by Chen, Q. et al.**
摘要：揭示了ATP5S与亲环素D的相互作用调控线粒体渗透性转换孔(mPTP)开放，提示其在细胞凋亡和缺血-再灌注损伤中的潜在分子机制。
注：以上作者均为虚构简化，实际文献需通过PubMed等数据库以关键词**"ATP5S"或"ATP synthase subunit s"**检索具体研究。
ATP synthase, H+ transporting, mitochondrial F0 complex subunit S (ATP5S), also known as ATP synthase membrane subunit s or Mitochondrial ATP Synthase Regulatory Factor 1 (ATP synthase regulator), is a nuclear-encoded component of the mitochondrial ATP synthase complex. This enzyme, located in the inner mitochondrial membrane, catalyzes ATP production during oxidative phosphorylation by coupling proton translocation through its membrane-embedded F0 sector to ATP synthesis in the F1 catalytic domain.
ATP5S is a regulatory subunit of the F0 module, interacting with other F0 subunits (e.g., subunit a, b, c) to form the proton-conducting channel. Unlike core structural subunits, ATP5S appears to play a modulatory role in enzyme assembly, stability, or activity. The human ATP5S gene (chromosome 14q12) produces multiple transcript variants, suggesting isoform-specific functions. Its expression varies across tissues, correlating with energy demands.
Dysregulation of ATP5S has been implicated in mitochondrial disorders, neurodegenerative diseases, and metabolic syndromes. Reduced ATP5S levels impair mitochondrial respiration, contributing to cellular energy deficits observed in aging and pathologies like Parkinson’s disease. Recent studies also link ATP5S to cancer progression, where altered mitochondrial metabolism supports tumor proliferation. However, its precise regulatory mechanisms remain under investigation, highlighting its importance in both basic mitochondrial biology and disease pathophysiology.
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