Cat.No. : CSC-RO0293 Host Cell: CHO-K1
| Cat. No. | CSC-RO0293 |
| Description | CHO- ACE2 cell line stably overexpresses human angiotensin I converting enzyme 2 (ACE2). It is a useful tool for in vitro screening and characterization of potential drugs against SARS-CoV, SARS-Cov2 (2019-nCoV). |
| Gene | ACE2 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | CHO-K1 |
| Host Cell Species | Cricetulus griseus (Chinese hamster) |
| Stability | Validated for at least 10 passages |
| Application | 1. Study the mechanisms of viral entry and replication 2. Research and in vitro screening of potential drugs 3. Vaccine development 4. The production of pseudotyped viruses |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Shipping | Dry ice |
| Storage | Liquid nitrogen |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Angiotensin-converting enzyme 2 (ACE2) antagonizes angiotensin II (Ang-II) by converting it to Ang-(1–7), but the effects of ACE2 and Ang-(1–7) on endothelial cell function and the evolution of atherosclerosis remain unclear. Researchers used a recombinant adenoviral vector to locally overexpress the ACE2 gene in human endothelial cells in vitro and apoE-deficient mice in vivo. The study showed that ACE2 gene transfer not only promoted HUVECs migration, inhibited monocyte adhesion, and reduced Ang II-induced MCP-1, VCAM-1, and E-selectin protein production in vitro, but also reduced MCP-1, VCAM-1, and interleukin-6 levels in vivo, inhibiting atherosclerotic plaque evolution. In addition, A779 administration increased MCP-1, VCAM-1, and interleukin-6 levels in vivo, leading to further aggravation of atherosclerosis.
Here, the effect of ACE2 on HUVECs migration was studied. The results showed that ACE2 overexpression (Ad-ACE2) promoted the migration of HUVECs compared with Ad-EGFP or the control group (Figure 1a, b), while A779 partially reversed the effect of ACE2 overexpression on HUVECs migration. The results showed that ACE2 can improve endothelial cell activity, and Ang-(1–7) plays an important role in protecting endothelial cell activity. The researchers also evaluated the effect of ACE2 overexpression on the adhesion of U-937 to HUVECs, and the results showed that the adhesion of U-937 to HUVECs in the Ad-ACE2 group was significantly lower than that in the AdEGFP or control group. In contrast, A779 partially reversed the effect of U-937 adhesion to HUVECs in the Ad-ACE2+A779 group (Figure 1c).
Figure 1. HUVECs migration assay and adhesion of U-937 cells to HUVECs. a HUVECs migration assay in ACE2 overexpression cell. b Quantitative evaluation of HUVECs migration. (Zhang Y H, et al., 2015)
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Incorporating the human ACE2 stable cell line has made our virus-host interaction studies much more relevant and insightful. The physiological relevance of our experiments has improved, providing us with more meaningful and actionable data.
This product excels in transfection efficiency compared to other cell lines we have tried. The stable expression of ACE2 has led to a significant improvement in our experimental outcomes, particularly in screening assays for antiviral compounds.
The technical support team has been fantastic. They responded promptly to our inquiries and provided detailed guidance, which was particularly helpful during the initial setup.
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