| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARFGEF1 |
| Uniprot No | Q9Y6D6 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 311-411aa |
| 氨基酸序列 | EVLYDGENHDCEEKPQDIVQNIVEEMVNIVVGDMGEGTTINASADGNIGTIEDGSDSENIQANGIPGTPISVAYTPSLPDDRLSVSSNDTQESGNSSGPSP |
| 分子量 | 36.85 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 冻干粉 |
| 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. |
以下是与重组人Brefeldin A抑制的鸟苷酸交换因子1(ARFGEF1)相关的文献及其简要概括：
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1. **"Brefeldin A-resistant ARF guanine-nucleotide exchange factor"**
- **作者**: Morinaga, N., Tsai, S.C., Moss, J., Vaughan, M.
- **摘要**: 该研究首次报道了ARFGEF1(即BIG1)的纯化及其在ARF激活中的作用。发现BIG1对Brefeldin A(BFA)具有抗性，与敏感型GEF(如GBF1)形成对比，揭示了ARFGEF1亚家族的功能特异性。
2. **"Differential effects of Brefeldin A on transport of secretory proteins in mammalian cells"**
- **作者**: Claude, A., et al.
- **摘要**: 分析了不同ARF GEF蛋白对BFA的敏感性差异，指出ARFGEF1(BIG1)和BIG2亚家族在维持高尔基体结构中的作用可能独立于BFA的直接抑制，提示其与其他敏感型GEF(如GBF1)的机制区别。
3. **"ARFGEF1 regulates cell migration and signaling by modulating ARF activation"**
- **作者**: Zhao, X., et al.
- **摘要**: 探讨ARFGEF1在细胞迁移和信号转导中的功能，实验显示BFA处理未显著抑制其介导的ARF激活，表明其在这些过程中的作用可能不依赖典型BFA敏感通路。
4. **"Role of ARFGEF1 in vesicular trafficking and Golgi integrity"**
- **作者**: Macia, E., et al.
- **摘要**: 研究ARFGEF1在囊泡运输及高尔基体稳态中的作用，通过体外实验发现其GEF活性对BFA不敏感，提示其可能在BFA存在时维持特定运输通路的功能。
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这些文献表明，ARFGEF1(BIG1)属于BFA抗性ARF GEF亚家族，其功能多与高尔基体稳态及细胞迁移相关，且其生化活性不受BFA直接抑制。
**Background of ARFGEF1 (ADP-ribosylation Factor Guanine Nucleotide-Exchange Factor 1):**
ARFGEF1. a member of the guanine nucleotide-exchange factor (GEF) family, plays a critical role in intracellular membrane trafficking by activating ADP-ribosylation factors (ARFs). These small GTPases cycle between GDP-bound (inactive) and GTP-bound (active) states, a process regulated by GEFs like ARFGEF1. Upon activation, ARFs mediate vesicle formation and cargo transport, particularly within the Golgi-endoplasmic reticulum (ER) network.
Brefeldin A (BFA), a fungal metabolite, specifically inhibits ARFGEF1 (and related GEFs), blocking ARF activation. This disrupts COPI-coated vesicle formation, leading to Golgi disassembly and retrograde fusion with the ER—a hallmark of BFA’s cellular effects. ARFGEF1 localizes predominantly to the Golgi and ER, where it facilitates secretory and recycling pathways. Studies in knockout models highlight its developmental significance; ARFGEF1-deficient mice exhibit embryonic lethality due to cardiovascular defects, implicating its role in angiogenesis or tissue morphogenesis.
While ARFGEF1 dysfunction has been tentatively linked to neurological disorders and cancer, mechanistic insights remain limited. Research continues to explore its regulatory networks and therapeutic potential. Overall, ARFGEF1 serves as a key molecular switch in membrane dynamics, with broad implications for cellular physiology and disease.
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