C5aR1/β-Arrestin/CHO
CBP71384
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| I. Background | |
| 补体 C5a 是由补体系统经 C5 转化酶裂解 C5 产生的强效炎症介质，作为核心过敏毒素 顺利获得结合受体 C5aR1/C5aR2 驱动中性粒细胞趋化、氧化爆发及炎性因子（IL-6/TNF-α）释 放，在脓毒症中诱发“细胞因子风暴”，在自身免疫病（如类风湿关节炎）中促进组织侵 蚀，在肿瘤微环境募集髓系抑制细胞（MDSC）介导免疫逃逸。 C5aR1（CD88）是补体过敏毒素 C5a 的高亲和力 GPCR，主要表达于髓系细胞（中性 粒细胞、单核细胞、肥大细胞），顺利获得激活 Gi/Gq 蛋白-PI3K/MAPK 通路驱动炎症级联反 应。 |
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| II. Description | |
C5aR1 β-Arrestin CHO 报告基因药靶模型很好的模拟了体内 C5aR1/β-Arrestin 的信号转导过程，原理见下图所示。 Figure 1. C5aR1 β-Arrestin CHO 细胞模型原理图 |
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| III. Introduction | |
| Expressed gene: |
C5aR1 |
| Stability: | 32 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.) |
| Freeze Medium: | 90% FBS+10% DMSO |
| Culture Medium: | F12K+10%FBS+5 μg/ml Puromycin+5 μg/ml Blasticidin |
| Mycoplasma Status: | Negative |
| Storage: | Liquid nitrogen immediately upon delivery |
| Application(s): |
Functional assay for C5aR1 |
| Transducer: | β-Arrestin |
| IV. Description of Host Cell Line | |
| Organism: | Hamster |
| Tissue: | Ovary |
| Morphology: | Epithelial |
| Growth Properties: | Adherent |
| V. Representative Data | |
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Figure 3. Dose Response of Human C5a in C5aR1 β-Arrestin CHO (C8). |
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Figure 4. Inhibition of hC5a-induced Beta-Arrestin Recruitment by hC5a Neutralization Ab in C5aR1 β-Arrestin CHO(C8). |
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