| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | AP4b1 |
| Uniprot No | Q9Y6B7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-739aa |
| 氨基酸序列 | MPYLGSEDVV KELKKALCNP HIQADRLRYR NVIQRVIRYM TQGLDMSGVF MEMVKASATV DIVQKKLVYL YMCTYAPLKP DLALLAINTL CKDCSDPNPM VRGLALRSMC SLRMPGVQEY IQQPILNGLR DKASYVRRVA VLGCAKMHNL HGDSEVDGAL VNELYSLLRD QDPIVVVNCL RSLEEILKQE GGVVINKPIA HHLLNRMSKL DQWGQAEVLN FLLRYQPRSE EELFDILNLL DSFLKSSSPG VVMGATKLFL ILAKMFPHVQ TDVLVRVKGP LLAACSSESR ELCFVALCHV RQILHSLPGH FSSHYKKFFC SYSEPHYIKL QKVEVLCELV NDENVQQVLE ELRGYCTDVS ADFAQAAIFA IGGIARTYTD QCVQILTELL GLRQEHITTV VVQTFRDLVW LCPQCTEAVC QALPGCEENI QDSEGKQALI WLLGVHGERI PNAPYVLEDF VENVKSETFP AVKMELLTAL LRLFLSRPAE CQDMLGRLLY YCIEEEKDMA VRDRGLFYYR LLLVGIDEVK RILCSPKSDP TLGLLEDPAE RPVNSWASDF NTLVPVYGKA HWATISKCQG AERCDPELPK TSSFAASGPL IPEENKERVQ ELPDSGALML VPNRQLTADY FEKTWLSLKV AHQQVLPWRG EFHPDTLQMA LQVVNIQTIA MSRAGSRPWK AYLSAQDDTG CLFLTELLLE PGNSEMQISV KQNEARTETL NSFISVLETV IGTIEEIKS |
| 预测分子量 | 83,2 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AP4B1重组蛋白的3篇参考文献示例(文献信息为模拟概括，建议通过学术数据库核实)：
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1. **文献名称**: *"AP4B1 mutations disrupt lysosomal protein trafficking and cause hereditary spastic paraplegia"*
**作者**: Hirst J, et al.
**摘要**: 研究通过重组AP4B1蛋白表达，揭示了其作为AP4复合体亚基在溶酶体蛋白运输中的作用，突变导致复合体功能丧失，引发神经退行性病理表型。
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2. **文献名称**: *"Functional characterization of AP4B1 in neuronal vesicle transport using recombinant protein models"*
**作者**: Bürgermeister J, et al.
**摘要**: 利用重组AP4B1蛋白进行体外结合实验，证明其与特异性信号肽相互作用，调控神经元内囊泡运输，突变体导致轴突运输障碍。
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3. **文献名称**: *"Recombinant AP4B1 expression and interaction network analysis in adaptor protein complexes"*
**作者**: Keren H, et al.
**摘要**: 通过重组AP4B1蛋白的纯化与结构分析，解析了其在AP4复合体中的结合位点，为遗传性痉挛性截瘫的分子机制提供了结构生物学证据。
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**提示**：以上内容为基于AP4B1已知功能的模拟概括，实际文献需通过PubMed、Google Scholar等平台检索确认。建议使用关键词 **"AP4B1 recombinant"** 或 **"AP4 adaptor complex"** 查找最新研究。
The AP4B1 gene encodes the beta-1 subunit of the Adaptor Protein Complex 4 (AP-4), a conserved heterotetrameric complex involved in intracellular vesicle trafficking. AP-4 facilitates the formation of transport vesicles and cargo sorting at the trans-Golgi network (TGN), primarily mediating selective protein transport to autophagosomes, lysosomes, and the cell membrane. It plays critical roles in neuronal development, synaptic function, and maintaining cellular homeostasis by regulating the sorting of transmembrane proteins, including autophagy-related receptors and neurotransmitter receptors.
Mutations in AP4B1 are linked to autosomal recessive hereditary spastic paraplegia 48 (SPG48), a neurodegenerative disorder characterized by progressive lower limb spasticity, intellectual disability, and developmental delays. This underscores AP4B1's importance in neuronal maintenance. Studying AP4B1 dysfunction provides insights into mechanisms of axonal degeneration and lysosomal trafficking defects.
Recombinant AP4B1 protein is engineered using expression systems (e.g., E. coli, mammalian cells) to produce purified, functional protein for mechanistic studies. It enables in vitro analysis of AP-4 complex assembly, interactions with cargo proteins, and vesicle formation dynamics. Researchers utilize this tool to investigate disease-associated mutations, screen therapeutic compounds, and develop model systems for SPG48. Its applications extend to elucidating broader AP-4 biology and validating gene therapy strategies targeting AP4B1 deficiencies. By bridging molecular insights with clinical phenotypes, recombinant AP4B1 accelerates both basic research and translational efforts in neurogenetic disorders.
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