| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RAB39B |
| Uniprot No | Q96DA2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-213aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMEAIWLY QFRLIVIGDS TVGKSCLIRR FTEGRFAQVS DPTVGVDFFS RLVEIEPGKR IKLQIWDTAG QERFRSITRA YYRNSVGGLL LFDITNRRSF QNVHEWLEET KVHVQPYQIV FVLVGHKCDL DTQRQVTRHE AEKLAAAYGM KYIETSARDA INVEKAFTDL TRDIYELVKR GEITIQEGWE GVKSGFVPNV VHSSEEVVKS ERRCLC |
| 预测分子量 | 27 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RAB39B重组蛋白研究的3篇代表性文献(示例为模拟内容，实际文献需根据数据库核实)：
---
1. **文献名称**: "RAB39B mutations impair protein transport and cause X-linked Parkinsonism"
**作者**: Wilson GR, et al.
**摘要**: 本研究通过重组RAB39B蛋白表达及体外功能实验，发现致病性突变(如p.Arg192Cys)会破坏其GTPase活性，导致囊泡运输障碍，从而阐明其在X连锁帕金森综合征中的分子机制。
2. **文献名称**: "Structural characterization of recombinant RAB39B and its interaction with SCAMP5"
**作者**: Li X, et al.
**摘要**: 利用大肠杆菌系统表达并纯化重组RAB39B蛋白，通过X射线晶体学解析其三维结构，揭示了其与SCAMP5蛋白的结合界面，为神经发育障碍相关通路研究提供结构基础。
3. **文献名称**: "RAB39B regulates neuronal synaptic vesicle trafficking via recombinant protein interaction assays"
**作者**: Chen L, et al.
**摘要**: 通过重组RAB39B与突触小泡标记蛋白(如VAMP2)的体外互作实验，证明其通过调控囊泡锚定影响神经递质释放，为智力障碍相关突触功能障碍提供证据。
---
**注**：以上文献信息为示例，实际引用时建议通过PubMed或Web of Science以关键词“RAB39B recombinant”检索近5年文献，优先选择《Nature Cell Biology》《Human Molecular Genetics》等期刊的高影响力研究。
**Background of RAB39B Recombinant Protein**
RAB39B is a member of the RAB family of small GTPases, which play critical roles in regulating intracellular vesicular trafficking, membrane dynamics, and cargo transport. Specifically, RAB39B is implicated in controlling Golgi apparatus organization, autophagy, and synaptic vesicle maturation. It is predominantly expressed in the brain, particularly in neurons and microglia, suggesting its importance in neurodevelopment and neurological function.
Genetic studies have linked mutations in the *RAB39B* gene to neurodevelopmental disorders, including X-linked intellectual disability, autism spectrum disorders, and early-onset Parkinson’s disease. Loss-of-function mutations disrupt RAB39B’s ability to cycle between active (GTP-bound) and inactive (GDP-bound) states, impairing its interaction with downstream effectors. This dysregulation is associated with defective α-synuclein homeostasis, aberrant neurotransmitter release, and pathological protein aggregation, all hallmarks of neurodegenerative conditions.
Recombinant RAB39B protein is engineered using heterologous expression systems (e.g., *E. coli* or mammalian cells) to produce purified, functional protein for mechanistic studies. It typically includes affinity tags (e.g., His-tag) for easy purification and detection. Researchers utilize this tool to investigate RAB39B’s structure, GTPase activity, binding partners, and role in cellular pathways. Its application extends to drug screening assays aiming to modulate RAB39B activity or rescue trafficking defects in disease models.
Overall, RAB39B recombinant protein serves as a vital resource for unraveling molecular mechanisms underlying neurological disorders and developing targeted therapeutic strategies.
×
