纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | Ang1-7 |
Uniprot No | P03950 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 26-147aa |
氨基酸序列 | DNSRYTHFLTQHYDAKPQGRDDRYCESIMRRRGLTSPCKDINTFIHGNKRSIKAICENKNGNPHRENLRISKSSFQVTTCKLHGGSPWPPCQYRATAGFRNVVVACENGLPVHLDQSIFRRP |
预测分子量 | 18.0 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Ang1-7重组蛋白的参考文献示例(文献信息为模拟概括,建议通过学术数据库查询具体内容):
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1. **文献名称**: *Recombinant Angiotensin-(1-7) attenuates hypertension and cardiac fibrosis in experimental models*
**作者**: Santos RA, et al.
**摘要**: 研究通过基因重组技术制备Ang1-7.验证其在高血压动物模型中降低血压和抑制心肌纤维化的效果,证实其通过Mas受体介导的抗氧化和抗炎途径发挥作用。
2. **文献名称**: *Therapeutic potential of recombinant Ang-(1-7) in pulmonary fibrosis via modulation of TGF-β signaling*
**作者**: Li Y, et al.
**摘要**: 探讨重组Ang1-7对肺纤维化小鼠模型的干预作用,发现其通过抑制TGF-β/Smad信号通路减少胶原沉积,改善肺功能,提示其作为抗纤维化药物的潜力。
3. **文献名称**: *Efficient production of recombinant Angiotensin-(1-7) in E. coli and its renoprotective effects in diabetic nephropathy*
**作者**: Zhang H, et al.
**摘要**: 报道一种利用大肠杆菌高效表达重组Ang1-7的工艺,并在糖尿病肾病模型中验证其减少蛋白尿、保护肾小球功能的机制,涉及ACE2/MasR轴激活。
4. **文献名称**: *Ang-(1-7) reduces inflammation and endothelial dysfunction in atherosclerosis via NLRP3 inflammasome inhibition*
**作者**: Patel VB, et al.
**摘要**: 研究重组Ang1-7对动脉粥样硬化斑块的影响,发现其通过抑制NLRP3炎性小体和改善内皮功能延缓疾病进展。
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**备注**:以上为模拟文献摘要,实际研究需通过PubMed、Web of Science等平台检索关键词如“recombinant Angiotensin-(1-7)”、“Ang1-7 therapeutic application”获取具体文献。
Angiotensin-(1-7) [Ang1-7] is a bioactive peptide component of the renin-angiotensin system (RAS), initially identified as a counter-regulatory fragment opposing the classical ACE/Ang II/AT1R axis. Derived primarily through ACE2-mediated cleavage of angiotensin II (Ang II), Ang1-7 binds selectively to the G protein-coupled Mas receptor (MasR), triggering signaling pathways associated with vasodilation, anti-inflammatory effects, and organ protection. This heptapeptide gained scientific prominence as researchers uncovered its role in mitigating pathological processes like hypertension, fibrosis, and oxidative stress.
The development of recombinant Ang1-7 protein emerged to address limitations of synthetic peptide administration, including rapid enzymatic degradation (half-life <30 minutes) and poor tissue penetration. Recombinant production systems (e.g., E. coli, yeast, or mammalian cell lines) enable scalable synthesis with post-translational modifications to enhance stability. Typical strategies involve fusion tags like thioredoxin or SUMO to improve solubility, followed by enzymatic cleavage and chromatographic purification.
Research highlights Ang1-7's therapeutic potential across cardiovascular diseases (heart failure, atherosclerosis), metabolic disorders (diabetes-induced nephropathy), and acute lung injuries, including COVID-19-related complications. Preclinical models demonstrate its capacity to reduce myocardial hypertrophy, improve endothelial function, and suppress pro-fibrotic cytokines. Notably, its anti-thrombotic and anti-arrhythmic properties differentiate it from conventional RAS inhibitors.
Current challenges involve optimizing delivery methods (nanoparticles, sustained-release formulations) and defining dosage regimens for clinical translation. As a research tool, recombinant Ang1-7 facilitates mechanistic studies of the ACE2/Ang1-7/MasR axis, particularly in diseases where RAS imbalance contributes to pathogenesis. Ongoing trials explore its efficacy in pulmonary hypertension and chronic kidney disease, positioning it as a promising candidate for next-generation RAS modulation therapies.
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