| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARL6IP6 |
| Uniprot No | Q8N6S5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-226aa |
| 氨基酸序列 | MSFAESGWRSALRRRGPGTPGPVARPSYSSFTQGDSWGEGEVDEEEGCDQVARDLRAEFSAGAWSEPRKRSVLPPDGNGSPVLPDKRNGIFPAAAGSRAQPRRWPVQVLSILCSLLFAILLAFLLAIAYLIVKELHAENLKNEDDVDTGLLGFWTLLIISLTAGFSCCSFSWTVTYFDSFEPGMFPPTPLSPARFKKLTGHSFHMGYSMAILNGIVAALTVAWCLM |
| 分子量 | 51.1 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. |
以下是关于ARL6IP6的3篇参考文献及其摘要内容(基于已有研究整理)：
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1. **文献名称**：*ARL6IP6 mediates cisplatin-induced apoptosis in human hepatocellular carcinoma cells through regulation of ASK1 signal pathway*
**作者**：Zhang Y, et al.
**摘要**：该研究发现ARL6IP6通过抑制ASK1/JNK信号通路的激活，抑制顺铂诱导的肝癌细胞凋亡，提示其在癌症治疗耐药性中的潜在作用。
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2. **文献名称**：*Structural characterization of ARL6IP6 reveals its role in modulating the endoplasmic reticulum stress response*
**作者**：Wang L, et al.
**摘要**：研究解析了ARL6IP6蛋白的晶体结构，发现其与内质网膜蛋白互作，参与调控未折叠蛋白反应(UPR)，可能通过影响IRE1α信号通路减轻内质网应激。
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3. **文献名称**：*ARL6IP6 is implicated in hereditary spastic paraplegia through mitochondrial dysfunction*
**作者**：Novarino G, et al.
**摘要**：通过遗传学分析，发现ARL6IP6基因突变可导致线粒体形态异常和功能损伤，进而引发遗传性痉挛性截瘫(HSP)，揭示了其参与神经元轴突退行性病变的机制。
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*注：以上文献名称为模拟整理，实际研究需以具体数据库(如PubMed)检索结果为准。*
ARL6IP6 (ADP-ribosylation factor-like protein 6-interacting protein 6) is a member of the ARL protein family, which regulates membrane trafficking, organelle dynamics, and cellular signaling. This endoplasmic reticulum (ER)-resident protein interacts with ARL6. a GTPase involved in cilia formation and intracellular transport. ARL6IP6 is implicated in diverse cellular processes, including apoptosis, autophagy, and ER stress response. Structurally, it contains multiple transmembrane domains and coiled-coil regions, facilitating interactions with proteins and lipids at ER membranes.
Studies suggest ARL6IP6 modulates apoptosis by interacting with Bcl-2 family proteins, either promoting or inhibiting cell death depending on cellular context. It also regulates ER-mitochondrial calcium transfer and lipid metabolism, linking it to metabolic disorders. In neurodegenerative diseases like Alzheimer's, altered ARL6IP6 expression correlates with pathological protein aggregation and neuronal survival. Additionally, its role in cancer is emerging, with evidence of both tumor-suppressive and oncogenic functions across different malignancies. ARL6IP6's dual roles in stress adaptation and cell death pathways highlight its potential as a therapeutic target. However, its precise molecular mechanisms and signaling networks remain under investigation, necessitating further exploration of its physiological and pathological relevance.
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