| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARL6IP5 |
| Uniprot No | O75915 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-64aa |
| 氨基酸序列 | MDVNIAPLRAWDDFFPGSDRFARPDFRDISKWNNRVVSNLLYYQTNYLVVAAMMISIVGFLSPF |
| 分子量 | 32.78 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. |
1. **"ARL6IP5 mediates cross-talk between the neural dysfunction and metabolic inflammation in Parkinson’s disease"**
- 作者：Zhang X, et al.
- 摘要：研究揭示了ARL6IP5在帕金森病中通过调节线粒体功能与炎症反应，影响神经元代谢与免疫应答的分子机制。
2. **"ARL6IP5 interacts with JWA to regulate cell apoptosis via the ER stress pathway"**
- 作者：Chen Y, et al.
- 摘要：通过体外实验验证ARL6IP5与JWA蛋白相互作用，通过内质网应激通路(如调控ATF6和XBP1)抑制氧化应激诱导的细胞凋亡。
3. **"ARL6IP5 deficiency enhances neuronal vulnerability to ALS-linked oxidative stress"**
- 作者：Ferguson C, et al.
- 摘要：在小鼠模型中证明ARL6IP5缺失加剧肌萎缩侧索硬化症(ALS)相关的神经元氧化损伤，提示其抗氧化与神经保护功能。
4. **"Structural basis of ARL6IP5-mediated sphingolipid transport in lysosomes"**
- 作者：Liu Q, et al.
- 摘要：解析ARL6IP5蛋白结构，揭示其通过结合鞘脂类分子调控溶酶体脂质代谢的新机制，为溶酶体贮积症研究提供依据。
(注：以上文献信息为示例，实际引用请核对PubMed等数据库获取原文。)
ADP-ribosylation factor-like 6-interacting protein 5 (ARL6IP5), also known as PRAF3 or SPG61. is a member of the PRA1 family involved in membrane trafficking and apoptosis regulation. Structurally, it contains conserved transmembrane domains localizing primarily to the endoplasmic reticulum (ER) and nuclear envelope. Functionally, ARL6IP5 modulates apoptosis by interacting with Bcl-2 family proteins, particularly inhibiting Bax activation to suppress mitochondrial apoptosis pathways. It also participates in ER morphology maintenance and vesicular transport through associations with small GTPases like ARL6.
Genetically, ARL6IP5 mutations are linked to hereditary spastic paraplegia type 61 (SPG61), a neurodegenerative disorder characterized by progressive lower limb spasticity. Dysregulation of ARL6IP5 has been implicated in cancer, where its reduced expression correlates with poor prognosis in glioblastoma and resistance to chemotherapy. Additionally, it interacts with survival motor neuron (SMN) proteins, suggesting a role in spinal muscular atrophy pathogenesis.
As a recombinant protein, ARL6IP5 is utilized to study its structural-functional relationships and therapeutic potential. Its dual roles in cellular trafficking and apoptosis make it a compelling target for neurodegenerative diseases and oncology research. However, mechanistic details of its pleiotropic functions remain under investigation, particularly regarding tissue-specific interactions and post-translational modifications.
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