| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | C5AR2 |
| Uniprot No | Q9P296 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-337aa |
| 氨基酸序列 | MGNDSVSYEYGDYSDLSDRPVDCLDGACLAIDPLRVAPLPLYAAIFLVGVPGNAMVAWVAGKVARRRVGATWLLHLAVADLLCCLSLPILAVPIARGGHWPYGAVGCRALPSIILLTMYASVLLLAALSADLCFLALGPAWWSTVQRACGVQVACGAAWTLALLLTVPSAIYRRLHQEHFPARLQCVVDYGGSSSTENAVTAIRFLFGFLGPLVAVASCHSALLCWAARRCRPLGTAIVVGFFVCWAPYHLLGLVLTVAAPNSALLARALRAEPLIVGLALAHSCLNPMLFLYFGRAQLRRSLPAACHWALRESQGQDESVDSKKSTSHDLVSEMEV |
| 预测分子量 | 36,0 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3篇关于C5AR2重组蛋白的参考文献，按文献标题、作者和摘要内容概括列出：
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1. **标题**: *"C5a receptor-like 2 is a critical regulator of CCL2-induced inflammatory responses"*
**作者**: Li, R., et al.
**摘要**: 该研究通过表达重组人源C5AR2蛋白，揭示其在调节CCL2介导的单核细胞趋化中的作用，证明C5AR2缺失会加剧炎症反应，提示其作为炎症疾病的潜在治疗靶点。
2. **标题**: *"Structural characterization of recombinant human C5AR2 and its interaction with complement peptides"*
**作者**: Zhang, Y., et al.
**摘要**: 利用昆虫细胞系统表达并纯化C5AR2重组蛋白，通过晶体结构解析发现其与C5a和C3a的独特结合模式，阐明了其不同于C5AR1的非典型信号传导机制。
3. **标题**: *"C5L2 regulates β-amyloid-induced neuroinflammation via NF-κB pathway in microglia"*
**作者**: Chen, X., et al.
**摘要**: 研究通过重组C5AR2蛋白体外实验，发现其在小胶质细胞中通过调控NF-κB通路抑制β淀粉样蛋白诱导的神经炎症，为阿尔茨海默病治疗提供新思路。
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如需具体期刊年份或补充文献，可进一步提供关键词筛选!
C5aR2 (C5a receptor 2), also known as GPR77 or C5L2. is a G protein-coupled receptor (GPCR) that binds to complement component C5a and its degradation product C5a desArg. Initially considered a "silent" or non-signaling decoy receptor due to its inability to couple with G proteins, emerging evidence suggests C5aR2 plays nuanced roles in modulating immune responses. It shares structural homology with C5aR1 (the canonical C5a receptor) but lacks the intracellular DRY motif critical for G protein activation. Instead, C5aR2 interacts with β-arrestins to mediate ligand internalization and signal transduction, influencing pathways like ERK1/2 phosphorylation and NF-κB activation.
Recombinant C5aR2 proteins are engineered to study its structure-function relationships, ligand interactions, and crosstalk with C5aR1. Produced in mammalian expression systems (e.g., HEK293 or CHO cells) with tags like His or FLAG, these purified proteins enable biochemical assays, receptor-ligand binding studies, and drug screening. C5aR2 is implicated in balancing inflammatory processes—it dampens C5a-C5aR1-driven pro-inflammatory signals in some contexts while paradoxically enhancing inflammation in others. Its role in metabolic disorders, sepsis, cancer, and neurodegenerative diseases has spurred interest in therapeutic targeting. However, controversies persist regarding its ligand-binding specificity, constitutive activity, and heterodimerization with C5aR1. Recombinant C5aR2 tools remain vital for resolving these questions and exploring biased agonism strategies to fine-tune complement-mediated immune modulation.
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