纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | HO1 |
Uniprot No | P09601 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-288aa |
氨基酸序列 | MERPQPDSMPQDLSEALKEATKEVHTQAENAEFMRNFQKGQVTRDGFKLV MASLYHIYVA LEEEIERNKESPVFAPVYFPEELHRKAALEQDLAFWYG PRWQEVIPYTPAMQRYVKRLHE VGRTEPELLVAHAYTRYLGDLSGGQV LKKIAQKALDLPSSGEGLAFFTFPNIASATKFKQ LYRSRMNSLEMTPA VRQRVIEEAKTAFLLNIQLFEELQELLTHDTKDQSPSRAPGLRQRA SN KVQDSAPVETPRGKPPLNTRSQAPLLRWVLTLSFLVATVAVGLYAM |
预测分子量 | 32 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3-4条模拟的关于HO1(Heme Oxygenase-1)重组蛋白研究的参考文献示例(实际文献需通过学术数据库查询):
---
1. **文献名称**: "Recombinant Human Heme Oxygenase-1: Expression, Purification, and Functional Characterization"
**作者**: Smith A, et al.
**期刊**: *Protein Expression and Purification*, 2018.
**摘要**: 研究报道了通过大肠杆菌表达系统高效表达重组人HO1蛋白的优化方法,包括纯化步骤和酶活性检测,证明其具有与天然蛋白相似的催化血红素降解的能力。
---
2. **文献名称**: "HO1 Recombinant Protein Attenuates Oxidative Stress in Murine Sepsis Models"
**作者**: Chen L, et al.
**期刊**: *Free Radical Biology and Medicine*, 2020.
**摘要**: 通过动物实验验证重组HO1蛋白对脓毒症小鼠氧化损伤的保护作用,发现其通过调控Nrf2通路减少炎症因子释放并改善器官功能。
---
3. **文献名称**: "Structural Insights into the Catalytic Mechanism of Recombinant Heme Oxygenase-1"
**作者**: Tanaka K, et al.
**期刊**: *Journal of Biological Chemistry*, 2019.
**摘要**: 利用X射线晶体学解析重组HO1蛋白的三维结构,揭示其血红素结合域的关键氨基酸残基及催化反应机制,为靶向药物设计提供依据。
---
4. **文献名称**: "Therapeutic Potential of Recombinant HO1 in Diabetic Nephropathy"
**作者**: Gupta R, et al.
**期刊**: *Cell Stress and Chaperones*, 2021.
**摘要**: 体外和体内实验表明,重组HO1蛋白可通过抑制肾细胞凋亡和纤维化改善糖尿病肾病,提示其作为新型治疗分子的潜力。
---
**注意**:以上文献信息为模拟示例,实际研究请通过PubMed、Web of Science或Google Scholar等平台检索关键词(如"recombinant HO1 protein" "heme oxygenase-1 expression")。
**Background of HO-1 Recombinant Protein**
Heme oxygenase-1 (HO-1), encoded by the *HMOX1* gene, is a cytoprotective enzyme that catalyzes the rate-limiting step in heme degradation, producing carbon monoxide (CO), biliverdin (later converted to bilirubin), and free iron. HO-1 is a stress-responsive protein induced by various stimuli, including oxidative stress, hypoxia, heavy metals, and inflammatory cytokines, primarily through the activation of the Nrf2-ARE (nuclear factor erythroid 2-related factor 2-antioxidant response element) pathway. Its antioxidant, anti-inflammatory, and anti-apoptotic properties make it a critical mediator of cellular adaptation to injury.
Recombinant HO-1 protein is produced using genetic engineering techniques, often expressed in *E. coli*, yeast, or mammalian cell systems. Purification typically involves affinity chromatography tags (e.g., His-tag) to ensure high yield and purity. The recombinant form retains the enzymatic activity of native HO-1. enabling its use in research and therapeutic applications.
HO-1 has garnered attention for its therapeutic potential in diseases involving oxidative stress and inflammation, such as atherosclerosis, neurodegenerative disorders, ischemia-reperfusion injury, and chronic kidney disease. Preclinical studies highlight its role in mitigating tissue damage and modulating immune responses. Additionally, HO-1-derived products (e.g., CO-releasing molecules) are being explored as therapeutics. Challenges include optimizing delivery methods, ensuring protein stability *in vivo*, and addressing context-dependent dual roles (e.g., pro-survival vs. potential pro-tumor effects). Current research focuses on enhancing recombinant HO-1's efficacy through nanoparticle delivery or gene therapy approaches, aiming to harness its cytoprotective benefits while minimizing off-target effects.
×