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Recombinant Human RAB6B protein

  • 中文名: RAS癌基因家族成员RAB6B(RAB6B)重组蛋白
  • 别    名: RAB6B;Ras-related protein Rab-6B
货号: PA1000-2635
Price: ¥询价
数量:
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产品详情

纯度>95%SDS-PAGE.
种属Human
靶点RAB6B
Uniprot NoQ9NRW1
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-208aa
氨基酸序列MGSSHHHHHH SSGLVPRGSH MSAGGDFGNP LRKFKLVFLG EQSVGKTSLI TRFMYDSFDN TYQATIGIDF LSKTMYLEDR TVRLQLWDTA GQERFRSLIP SYIRDSTVAV VVYDITNLNS FQQTSKWIDD VRTERGSDVI IMLVGNKTDL ADKRQITIEE GEQRAKELSV MFIETSAKTG YNVKQLFRRV ASALPGMENV QEKSKEGMID IKLDKPQEPP ASEGGCSC
预测分子量26 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.

参考文献

以下是关于RAB6B重组蛋白的虚构参考文献示例(仅供示例参考,非真实文献):

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1. **标题**: "Expression and GTPase Activity Analysis of Recombinant RAB6B Protein in Mammalian Cells"

**作者**: Chen L, et al.

**摘要**: 本研究利用哺乳动物表达系统成功表达了His标签的RAB6B重组蛋白,并通过亲和层析纯化。实验发现重组RAB6B在体外表现出依赖于镁离子的GTP水解活性,并证实其与已知效应蛋白BICD1的结合能力,为后续功能研究提供了基础。

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2. **标题**: "RAB6B Regulates Vesicular Trafficking via Interaction with COPI Complex: Insights from Recombinant Protein Assays"

**作者**: Martinez R, et al.

**摘要**: 通过重组RAB6B蛋白与COPI衣壳蛋白的体外结合实验,揭示了RAB6B在逆向高尔基体运输中的作用。研究利用表面等离子共振技术(SPR)量化了其结合动力学,并证明特定突变体(Q72L)导致持续激活,影响囊泡形成效率。

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3. **标题**: "Structural Characterization of Recombinant RAB6B in GDP- and GTP-Bound States by X-ray Crystallography"

**作者**: Watanabe K, et al.

**摘要**: 本研究首次解析了重组人源RAB6B蛋白在GDP和GTP类似物结合状态下的晶体结构,揭示了其Switch I/II区域构象变化如何调控效应蛋白识别,为靶向RAB6B的分子设计提供了结构基础。

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4. **标题**: "Role of Recombinant RAB6B in Autophagosome-Lysosome Fusion: Evidence from In Vitro Reconstitution"

**作者**: Gupta S, et al.

**摘要**: 通过体外重建实验,发现重组RAB6B蛋白与HOPS复合体协同促进自噬体-溶酶体膜融合。研究进一步证明,RAB6B的敲低导致细胞自噬流受阻,提示其在神经退行性疾病中的潜在病理机制。

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**注意**:以上文献为模拟示例,实际研究需通过PubMed、Google Scholar等平台检索真实文献(关键词如“RAB6B recombinant protein”“RAB6B GTPase”)。

背景信息

RAB6B is a member of the RAB family of small GTPases, which play critical roles in regulating intracellular vesicular trafficking and membrane dynamics. As a paralog of RAB6A, RAB6B shares structural similarity but exhibits distinct functional characteristics. It is primarily involved in retrograde transport pathways, facilitating the movement of vesicles from the Golgi apparatus to the endoplasmic reticulum (ER). This protein cycles between an active GTP-bound state and an inactive GDP-bound state, a process tightly regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs).

Recombinant RAB6B refers to the protein produced through genetic engineering in heterologous expression systems, such as *E. coli* or mammalian cell cultures. Its recombinant form allows for controlled studies of its biochemical properties, interaction partners, and regulatory mechanisms. Researchers often purify recombinant RAB6B to investigate its role in cellular processes like Golgi-ER trafficking, cytoskeletal organization, and autophagy. Structural studies of recombinant RAB6B, including its GTP-binding domains and post-translational modifications (e.g., prenylation), provide insights into its membrane association and functional specificity.

Dysregulation of RAB6B has been implicated in neurological disorders and cancer, making it a potential therapeutic target. Recombinant RAB6B proteins are essential tools for screening small-molecule modulators or studying mutations linked to disease. Additionally, they aid in mapping protein interaction networks using techniques like pull-down assays or yeast two-hybrid systems. By enabling precise manipulation and analysis, recombinant RAB6B contributes to understanding vesicular transport defects in pathologies and developing targeted interventions.

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