| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RAB39 |
| Uniprot No | Q14964 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-217 aa |
| 活性数据 | METIWIYQFR LIVIGDSTVG KSCLLHRFTQ GRFPGLRSPA CDPTVGVDFF SRLLEIEPGK RIKLQLWDTA GQERFRSITR SYYRNSVGGF LVFDITNRRS FEHVKDWLEE AKMYVQPFRI VFLLVGHKCD LASQRQVTRE EAEKLSADCG MKYIETSAKD ATNVEESFTI LTRDIYELIK KGEICIQDGW EGVKSGFVPN TVHSSEEAVK PRKECFC |
| 分子量 | 25.0 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. |
以下是关于重组人RAB39蛋白的3篇参考文献概述(注：文献为假设性示意，实际引用需核对真实数据库)：
1. **文献名称**: "Mutations in RAB39B cause X-linked intellectual disability and Parkinsonism"
**作者**: Giannandrea, M. et al. (2010)
**摘要**: 研究首次发现RAB39B基因突变与X连锁智力障碍和帕金森病相关，通过体外重组蛋白实验，揭示RAB39B调控突触囊泡运输和神经递质释放的分子机制。
2. **文献名称**: "RAB39B regulates α-synuclein pathology in Parkinson's disease"
**作者**: Wilson, G.R. et al. (2014)
**摘要**: 报道重组RAB39B蛋白在细胞模型中的作用，证明其缺失导致α-突触核蛋白异常聚集，提示RAB39B在帕金森病病理中的关键调控功能。
3. **文献名称**: "Structural and functional analysis of RAB39B in GTPase activity"
**作者**: Lara, J.A. et al. (2012)
**摘要**: 利用重组人RAB39B蛋白解析其晶体结构，阐明其GTP/GDP结合域的构象变化，揭示其作为小GTP酶在细胞内运输中的特异性作用机制。
建议通过PubMed或Google Scholar搜索实际文献，检索词如“recombinant RAB39B”或“RAB39B protein function”。
RAB39. a member of the Rab GTPase family, plays a critical role in regulating intracellular membrane trafficking, vesicle transport, and autophagy. This small GTPase cycles between GTP-bound (active) and GDP-bound (inactive) states, interacting with effector proteins to direct organelle-specific cargo sorting and membrane fusion. Human RAB39 exists as two isoforms: RAB39A and RAB39B, encoded by distinct genes. RAB39B, located on the X chromosome, has drawn particular attention due to its association with neurodevelopmental disorders. Loss-of-function mutations in RAB39B are linked to X-linked intellectual disability, autism spectrum disorders, and early-onset Parkinson’s disease, implicating its role in neuronal maintenance and synaptic vesicle dynamics. Studies suggest RAB39B influences α-synuclein homeostasis, with dysregulation potentially contributing to pathological protein aggregation. Structurally, RAB39B contains conserved GTPase domains and hypervariable C-terminal regions for membrane anchoring. While RAB39A's functions are less understood, it is implicated in inflammatory responses and glioblastoma progression. Current research focuses on deciphering RAB39 isoforms' distinct vesicular trafficking pathways, their interplay with neurodegenerative mechanisms, and therapeutic targeting. However, functional redundancies with other Rab proteins and tissue-specific expression patterns complicate mechanistic studies. Further characterization of RAB39’s interactome and signaling networks remains essential for understanding its pathophysiological roles.
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