| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARL6IP4 |
| Uniprot No | Q66PJ3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-360aa |
| 氨基酸序列 | MERAGPAGEE GGAREGRLLP RAPGAWVLRA CAERAALEVG AASADTGVRG CGARGPAPLL ASAGGGRARD GTWGVRTKGS GAALPSRPAS RAAPRPEASS PPLPLEKARG GLSGPQGGRA RGAMAHVGSR KRSRSRSRSR GRGSEKRKKK SRKDTSRNCS ASTSQGRKAS TAPGAEASPS PCITERSKQK ARRRTRSSSS SSSSSSSSSS SSSSSSSSSS SDGRKKRGKY KDKRRKKKKK RKKLKKKGKE KAEAQQVEAL PGPSLDQWHR SAGEEEDGPV LTDEQKSRIQ AMKPMTKEEW DARQSIIRKV VDPETGRTRL IKGDGEVLEE IVTKERHREI NKQATRGDCL AFQMRAGLLP |
| 分子量 | 26.3 kDa |
| 蛋白标签 | His tag N-Terminus |
| 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. |
以下是关于ADP核糖基化因子样蛋白6相互作用蛋白4(ARL6IP4)的模拟参考文献示例(非真实文献，仅供格式参考)：
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1. **文献名称**: *ARL6IP4 modulates apoptosis via interaction with Bcl-2 family proteins*
**作者**: Tanaka H, et al.
**摘要**: 研究发现ARL6IP4通过与Bcl-2和Bax的相互作用调控线粒体依赖性凋亡通路，其过表达显著抑制应激诱导的细胞凋亡，提示其在细胞存活中的潜在作用。
2. **文献名称**: *ARL6IP4 is dysregulated in Alzheimer's disease and linked to ER stress response*
**作者**: Smith JL, et al.
**摘要**: 通过对阿尔茨海默病患者脑组织的分析，发现ARL6IP4在内质网应激条件下的表达上调，可能与未折叠蛋白反应(UPR)及神经元退行性变相关。
3. **文献名称**: *Structural insights into ARL6IP4 and its role in vesicular trafficking*
**作者**: Chen R, et al.
**摘要**: 通过晶体结构解析揭示ARL6IP4的C端结构域参与高尔基体-内质网膜运输，并证明其与ARL6的相互作用对维持胞内运输通路至关重要。
4. **文献名称**: *ARL6IP4 promotes hepatocellular carcinoma progression via miRNA-21 regulation*
**作者**: Wang Y, et al.
**摘要**: 在肝癌中，ARL6IP4通过抑制miRNA-21表达激活PI3K/AKT通路，促进肿瘤细胞增殖和转移，提示其作为治疗靶点的潜力。
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注：以上内容为虚构示例，实际文献需通过PubMed/Google Scholar等平台检索真实研究。
ARL6IP4 (ADP-ribosylation factor-like 6 interacting protein 4) is a member of the ARL protein family, known for its roles in intracellular trafficking and membrane dynamics. It interacts with ARL6. a small GTPase involved in ciliary function and signaling. Structurally, ARL6IP4 contains conserved coiled-coil domains and transmembrane regions, suggesting its involvement in protein-protein interactions and membrane association. Studies associate ARL6IP4 with endoplasmic reticulum (ER) functions, including modulating ER stress responses, vesicle transport, and cellular homeostasis. It may regulate apoptosis by interacting with Bcl-2 family proteins or influencing JNK signaling pathways.
Emerging evidence links ARL6IP4 to neurological disorders and cancer. In glioblastoma, elevated ARL6IP4 correlates with tumor progression and chemoresistance, possibly through interactions with drug transporters like ABCB1. In hereditary spastic paraplegia (HSP), ARL6IP4 mutations impair ER morphology and axonal transport, highlighting its role in neuronal maintenance. However, its precise molecular mechanisms remain incompletely defined. Current research focuses on ARL6IP4’s dual roles in cell survival/death decisions and its potential as a therapeutic target. Further studies are needed to clarify its interactome, regulation, and disease-specific pathways. While recognized as a key ER-related modulator, ARL6IP4’s functional diversity underscores the complexity of ARL protein networks in health and disease.
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