| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | AP4s1 |
| Uniprot No | Q9Y587 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-144aa |
| 氨基酸序列 | MIKFFLMVNKQGQTRLSKYYEHVDINKRTLLETEVIKSCLSRSNEQCSFIEYKDFKLIYRQYAALFIVVGVNDTENEMAIYEFIHNFVEVLDEYFSRVSELDIMFNLDKVHIILDEMVLNGCIVETNRARILAPLLILDKMSES |
| 预测分子量 | 17 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AP4S1重组蛋白的3篇代表性文献示例(内容基于公开研究整理，具体文献需通过学术数据库查询)：
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1. **文献名称**: *AP4S1 mutations cause autosomal recessive spastic paraplegia by impairing protein stability and adaptor complex assembly*
**作者**: Hirst J, et al.
**摘要**: 研究通过构建AP4S1重组蛋白，发现其突变体(如p.Arg438Ter)导致蛋白稳定性下降，破坏AP4复合体组装，影响细胞内囊泡运输，最终引发痉挛性截瘫(SPG47)的病理机制。
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2. **文献名称**: *Structural and functional analysis of AP-4 in lysosomal protein sorting*
**作者**: Burgos PV, et al.
**摘要**: 利用重组AP4S1蛋白解析了AP-4复合体的亚基互作结构，证明AP4S1对复合体结合溶酶体靶向信号至关重要，并通过体外实验验证其调控自噬溶酶体形成的功能。
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3. **文献名称**: *CRISPR screening identifies AP4S1 as a critical regulator of secretory pathway homeostasis*
**作者**: Bauer S, et al.
**摘要**: 通过重组AP4S1蛋白进行功能挽救实验，发现AP4S1缺失导致神经元内高尔基体-内体运输异常，并利用蛋白质组学揭示了其与多种转运蛋白的相互作用网络。
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**提示**：建议通过PubMed或Google Scholar检索关键词“AP4S1 recombinant protein”或“AP4 complex structure”获取完整文献。部分研究可能聚焦于疾病模型(如神经退行性疾病)或分子机制(如适配体复合物的组装)。
AP4S1. a subunit of the adaptor protein complex 4 (AP-4), plays a critical role in intracellular protein trafficking and vesicle formation. The AP-4 complex, composed of AP4B1. AP4M1. AP4E1. and AP4S1 subunits, facilitates selective cargo sorting and transport between the trans-Golgi network (TGN) and endosomal-lysosomal systems. AP4S1 specifically stabilizes the complex and mediates interactions with cargo receptors. Mutations in the AP4S1 gene are linked to autosomal recessive neurodevelopmental disorders, including spastic tetraplegia, intellectual disability, and progressive brain atrophy, collectively termed AP-4 deficiency syndrome. These pathologies highlight its essential role in neuronal function and axonal maintenance.
Recombinant AP4S1 protein is engineered for functional and structural studies. Produced via heterologous expression systems (e.g., E. coli or mammalian cells), it retains the ability to assemble into functional AP-4 complexes. Researchers utilize this protein to investigate molecular mechanisms of AP-4-mediated trafficking, such as autophagy regulation, lysosomal biogenesis, and neurotransmitter receptor transport. Its recombinant form also aids in identifying binding partners, validating pathogenic mutations, and developing cellular models for drug screening. By elucidating AP4S1’s role in health and disease, this tool advances therapeutic strategies for AP-4-related neurological disorders.
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