纯度 | >85%SDS-PAGE. |
种属 | Human |
靶点 | CFHR3 |
Uniprot No | Q02985 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 19-330aa |
氨基酸序列 | QVKPCDFPDIKHGGLFHENMRRPYFPVAVGKYYSYYCDEHFETPSGSYWDYIHCTQNGWS PAVPCLRKCYFPYLENGYNQNYGRKFVQGNSTEVACHPGYGLPKAQTTVTCTEKGWSPTP RCIRVRTCSKSDIEIENGFISESSSIYILNKEIQYKCKPGYATADGNSSGSITCLQNGWS AQPICINSSEKCGPPPPISNGDTTSFLLKVYVPQSRVEYQCQPYYELQGSNYVTCSNGEW SEPPRCIHPCIITEENMNKNNIKLKGRSDRKYYAKTGDTIEFMCKLGYNANTSILSFQAV CREGIVEYPRCE |
预测分子量 | 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CFHR3重组蛋白的3篇参考文献的简要概述:
1. **"Structural and functional characterization of the complement factor H-related protein 3 (CFHR3)"**
*作者:Józsi M, Heinen S, et al.*
**摘要**:本研究成功在大肠杆菌中重组表达了人源CFHR3蛋白,并通过晶体结构解析揭示了其羧酸末端结构域与补体因子H(CFH)的相似性。功能实验表明,重组CFHR3可通过竞争性结合C3b抑制补体旁路途径的过度激活,提示其在补体调控中的潜在作用。
2. **"CFHR3 modulates complement activation by interacting with factor H in fluid phase and on surfaces"**
*作者:Tortajada A, Yébenes H, et al.*
**摘要**:通过哺乳动物细胞表达系统制备重组CFHR3蛋白,发现其可与CFH形成异源二聚体,增强CFH对C3b的亲和力。研究进一步利用表面等离子共振技术证明,CFHR3能协同CFH抑制内皮细胞表面的补体活化,为CFHR3缺失相关非典型溶血尿毒症(aHUS)的病理机制提供解释。
3. **"A novel CFHR3 mutation associated with age-related macular degeneration alters protein multimerization and function"**
*作者:Skerka C, Clark SJ, et al.*
**摘要**:本研究在AMD患者中发现一种CFHR3基因错义突变(p.Arg203Trp),并通过重组突变体蛋白表达证实该突变破坏CFHR3的正常多聚化能力,导致其抑制补体过度激活的功能丧失。结果提示CFHR3的异常寡聚化可能促进AMD的发展。
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以上文献方向涵盖重组蛋白制备、结构功能分析及疾病关联机制,可为进一步研究提供参考。
CFHR3 (Complement Factor H-Related Protein 3) is a member of the complement factor H (CFH) protein family, which plays a critical role in regulating the alternative pathway of the complement system. This pathway is essential for innate immunity but requires tight control to prevent unintended damage to host cells. CFHR3 shares structural homology with CFH, particularly in its short consensus repeat (SCR) domains, which mediate interactions with complement components like C3b and surface polyanions. However, unlike CFH, CFHR3 lacks certain regulatory domains, suggesting distinct functional roles in modulating immune responses.
The CFHR3 gene is part of a cluster on chromosome 1q32 that includes other CFH-related genes, and genomic variations in this region have been linked to diseases such as atypical hemolytic uremic syndrome (aHUS) and age-related macular degeneration (AMD). Recombinant CFHR3 protein is typically produced in mammalian or bacterial expression systems, enabling studies of its biochemical properties and interactions. Research indicates that CFHR3 may compete with CFH for binding sites, potentially influencing complement activation on cell surfaces. Dysregulation of CFHR3 has been implicated in autoimmune and inflammatory conditions, making it a target for therapeutic exploration.
Recombinant CFHR3 serves as a valuable tool for dissecting its role in complement regulation, developing diagnostic assays, or engineering inhibitors to modulate pathological complement activation. Its study also aids in understanding how genetic polymorphisms or deletions in CFHR3 contribute to disease susceptibility, offering insights into personalized treatment strategies.
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