| 纯度 | > 95 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARL3 |
| Uniprot No | P36405 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-182aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSHMGLLSILRKLKSAPDQEVRILLLGLD NAGKTTLLKQLASEDISHITPTQGFNIKSVQSQGFKLNVWDIGGQRKIRP YWKNYFENTDILIYVIDSADRKRFEETGQELAELLEEEKLSCVPVLIFAN KQDLLTAAPASEIAEGLNLHTIRDRVWQIQSCSALTGEGVQDGMNWVCKN VNAKKK |
| 预测分子量 | 23 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3-4条关于ARL3重组蛋白的参考文献示例(注：部分文献信息为虚构概括，实际文献需通过学术数据库验证)：
---
1. **文献名称**: *"Expression and Purification of Human ARL3 in a Bacterial System for Structural Studies"*
**作者**: Smith J, et al.
**摘要**: 该研究描述了在大肠杆菌中高效表达和纯化重组人源ARL3蛋白的方法，通过优化诱导条件和亲和层析技术获得高纯度蛋白，用于后续X射线晶体学分析，揭示其GTP结合结构域的构象变化。
2. **文献名称**: *"Functional Characterization of ARL3 Recombinant Protein in Ciliary Protein Trafficking"*
**作者**: Li X, et al.
**摘要**: 利用重组ARL3蛋白进行体外结合实验，发现其通过与转运伴侣UNC119的相互作用调控纤毛内脂修饰蛋白的定位，GTP水解活性对功能至关重要，为纤毛病机制研究提供依据。
3. **文献名称**: *"Cryo-EM Structure of ARL3-PDEδ Complex Reveals Membrane Association Mechanism"*
**作者**: Chen R, et al.
**摘要**: 通过冷冻电镜解析重组ARL3与效应蛋白PDEδ的复合物结构，阐明ARL3在GTP结合状态下如何介导PDEδ与细胞膜的结合，为靶向ARL3的药物设计提供结构基础。
4. **文献名称**: *"Role of ARL3 Recombinant Mutants in Retinal Degeneration: In Vitro Analysis"*
**作者**: Johnson K, et al.
**摘要**: 构建ARL3致病突变体(如T34K和L134P)的重组蛋白，发现突变导致GTP酶活性丧失和蛋白稳定性下降，揭示了ARL3缺陷引发视网膜变性的分子机制。
---
**提示**：以上文献内容为示例性质，实际研究中建议通过PubMed或Google Scholar搜索关键词“ARL3 recombinant”“ARL3 purification”“ARL3 structure”等获取真实文献。
ARL3 (ADP-ribosylation factor-like protein 3) is a small GTPase belonging to the ARF/ARL family, which plays critical roles in intracellular trafficking, lipid-modified protein localization, and ciliary function. Structurally, it alternates between inactive GDP-bound and active GTP-bound states, regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Unlike many ARF family members, ARL3 lacks membrane-targeting motifs, relying on interactions with cargo adaptors like PDE6D for spatial regulation.
Biologically, ARL3 is essential for shuttling lipidated proteins (e.g., prenylated or palmitoylated proteins) to cilia and photoreceptor outer segments. This function links it to retinal homeostasis, as mutations in ARL3 or its regulators cause inherited ciliopathies such as Joubert syndrome and autosomal recessive retinal dystrophies. Its role in regulating tubulin post-translational modifications further connects it to microtubule dynamics in specialized cellular compartments.
Recombinant ARL3 proteins are typically produced in bacterial (e.g., E. coli) or eukaryotic expression systems, often with solubility-enhancing tags like GST or His. Purified recombinant ARL3 enables structural studies (crystal/NMR structures), biochemical assays of nucleotide cycling, and screening for interactors through pull-down or SPR techniques. Engineered mutants (e.g., Q71L, GTP-locked; T31N, GDP-locked) help dissect its activation mechanisms.
Current research leverages recombinant ARL3 to develop therapeutic strategies for ciliary disorders and explore its potential as a drug target. Its conserved role across species makes it valuable for modeling human diseases in experimental systems.
×
