| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ORP150 |
| Uniprot No | Q9Y4L1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 695-994aa |
| 氨基酸序列 | MVEEIGVELV VLDLPDLPED KLAQSVQKLQ DLTLRDLEKQ EREKAANSLE AFIFETQDKL YQPEYQEVST EEQREEISGK LSAASTWLED EGVGATTVML KEKLAELRKL CQGLFFRVEE RKKWPERLSA LDNLLNHSSM FLKGARLIPE MDQIFTEVEM TTLEKVINET WAWKNATLAE QAKLPATEKP VLLSKDIEAK MMALDREVQY LLNKAKFTKP RPRPKDKNGT RAEPPLNASA SDQGEKVIPP AGQTEDAEPI SEPEKVETGS EPGDTEPLEL GGPGAEPEQK EQSTGQKRPL |
| 预测分子量 | 35 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. |
以下是关于ORP150重组蛋白的3篇参考文献及其简要摘要：
1. **标题**：*"Protective role of ORP150 in diabetic endothelial dysfunction through reduction of ER stress"*
**作者**：Ozawa K, et al.
**摘要**：该研究通过体外表达重组ORP150蛋白，发现其能显著降低高糖诱导的内皮细胞内质网应激(ER stress)和细胞凋亡，提示ORP150在糖尿病血管并发症中具有保护作用。
2. **标题**：*"Adenovirus-mediated overexpression of ORP150 improves cardiac function after ischemia-reperfusion injury"*
**作者**：Tamura Y, et al.
**摘要**：利用腺病毒载体在心肌细胞中表达重组ORP150蛋白，结果显示其通过抑制内质网应激相关通路，减少心肌缺血再灌注损伤后的细胞死亡，并改善心脏功能。
3. **标题**：*"Recombinant ORP150 alleviates neuronal apoptosis via modulating ER stress in a traumatic brain injury model"*
**作者**：Liu H, et al.
**摘要**：研究在小鼠脑损伤模型中注射重组ORP150蛋白，发现其通过减少内质网应激标志物(如CHOP和GRP78)的表达，显著抑制神经元凋亡并促进神经功能恢复。
4. **标题**：*"ORP150/HSP12A regulates oxidative stress in cerebral ischemia: Implications for recombinant protein therapy"*
**作者**：Kitao Y, et al.
**摘要**：该文献探讨重组ORP150蛋白在脑缺血模型中的作用，证明其通过清除活性氧(ROS)和稳定线粒体功能，减轻氧化应激导致的神经损伤。
这些研究均聚焦于重组ORP150蛋白在疾病模型中的保护机制，强调其通过调控内质网应激和氧化应激发挥治疗潜力。
ORP150 (Oxygen-Regulated Protein 150), also known as GRP170 or HYOU1. is a member of the heat shock protein (HSP) family localized in the endoplasmic reticulum (ER). Discovered in the 1990s, it is a 150 kDa chaperone protein encoded by the HYOU1 gene and plays a critical role in cellular stress responses, particularly under hypoxia, glucose deprivation, or ER stress. Structurally, it contains a substrate-binding domain and a nucleotide-binding domain, facilitating its interaction with misfolded proteins during the unfolded protein response (UPR).
ORP150 is upregulated under low-oxygen conditions, where it stabilizes nascent polypeptides, assists in protein folding, and prevents aggregation of denatured proteins. It also modulates ER stress signaling pathways, influencing cell survival or apoptosis. Its dual role in stress adaptation has linked it to pathologies such as ischemic injury, neurodegenerative diseases, and cancer. For instance, ORP150 overexpression in tumors promotes angiogenesis and chemoresistance, while its deficiency exacerbates neuronal damage post-stroke.
Recombinant ORP150 is typically produced using mammalian expression systems (e.g., HEK293 or CHO cells) or bacterial systems with optimized codon usage. Purification involves affinity chromatography, often leveraging histidine tags. Researchers utilize recombinant ORP150 to study ER stress mechanisms, develop diagnostic biomarkers, or explore therapeutic strategies. Preclinical studies highlight its potential in mitigating ischemic injuries or enhancing protein-folding efficiency in genetic disorders. However, its context-dependent pro-survival or cytotoxic effects necessitate careful evaluation in therapeutic applications.
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