| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RAB33B |
| Uniprot No | Q9H082 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-229aa |
| 氨基酸序列 | MAEEMESSLEASFSSSGAVSGASGFLPPARSRIFKIIVIGDSNVGKTCLTYRFCAGRFPDRTEATIGVDFRERAVEIDGERIKIQLWDTAGQERFRKSMVQHYYRNVHAVVFVYDMTNMASFHSLPSWIEECKQHLLANDIPRILVGNKCDLRSAIQVPTDLAQKFADTHSMPLFETSAKNPNDNDHVEAIFMTLAHKLKSHKPLMLSQPPDNGIILKPEPKPAMTCWC |
| 预测分子量 | 31.8 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RAB33B重组蛋白的3篇代表性文献摘要及作者信息：
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1. **文献名称**: "Rab33B regulates autophagy membrane dynamics through interaction with Atg16L1"
**作者**: Hirota Y, et al.
**摘要**: 该研究通过重组RAB33B蛋白的体外实验，揭示了其与自噬关键蛋白ATG16L1的直接结合作用，并证明RAB33B通过GTP酶活性调控自噬体膜的形成与延伸。
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2. **文献名称**: "Structural basis of Rab33B/RIC1-mediated membrane tethering in autophagy"
**作者**: Zhang X, et al.
**摘要**: 利用重组RAB33B蛋白的晶体结构解析，阐明了其与效应蛋白RIC1的互作机制，揭示了其在自噬过程中介导膜融合的分子基础，并验证了关键功能域突变对自噬活性的影响。
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3. **文献名称**: "Rab33B recruits the autophagic machinery to phagosomes for pathogen clearance"
**作者**: Wang J, et al.
**摘要**: 通过重组RAB33B蛋白的功能研究，发现其参与吞噬细胞清除病原体的过程，通过招募LC3等自噬相关蛋白至吞噬体膜，促进吞噬体-溶酶体融合及病原体降解。
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**备注**：若需获取具体文献，可通过PubMed或Sci-Hub输入标题/作者查询全文。建议结合研究场景(如自噬、膜运输或疾病模型)进一步筛选文献。
RAB33B is a member of the Rab GTPase family, which regulates intracellular membrane trafficking by cycling between active GTP-bound and inactive GDP-bound states. It localizes primarily to the Golgi apparatus and plays a critical role in maintaining Golgi structure, autophagosome formation, and vesicle-mediated transport. RAB33B is implicated in mediating cargo selection, vesicle budding, and fusion events, particularly in pathways connecting the Golgi with the endoplasmic reticulum or lysosomes. Dysregulation of RAB33B is linked to human diseases, including cancer, neurodegenerative disorders, and rare genetic conditions like X-linked congenital cataracts. Its involvement in autophagy—a process crucial for cellular homeostasis—has drawn attention in cancer research and neurodegeneration studies.
Recombinant RAB33B protein, produced using expression systems like *E. coli* or mammalian cells, enables functional studies in vitro. These purified proteins often include tags (e.g., His-tag) for affinity chromatography and may be pre-loaded with GTP/GDP to study conformational changes. Researchers use recombinant RAB33B to investigate its interactions with effector proteins (e.g, ATG16L1 in autophagy), GTPase-activating proteins (GAPs), or guanine nucleotide exchange factors (GEFs). Structural analyses (e.g., crystallography) and enzymatic assays (GTP hydrolysis kinetics) rely on high-purity recombinant forms. Disease-associated mutations (e.g., G77R in congenital cataracts) are recreated in recombinant proteins to dissect mechanistic impacts. Additionally, recombinant RAB33B aids in drug discovery screens targeting autophagy-related pathways or membrane trafficking defects. Its study advances understanding of cellular trafficking networks and their roles in health and disease.
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