ArticleFEMS immunology and medical microbiology2006
Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.
Article in FEMS immunology and medical microbiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- The structure and function of membrane protein in coronavirus infection and its applications in the development of vaccines and therapeutic drugs.Frontiers in microbiology · 2026Review
- Treadmill Exercise Modulates the Leptin/LepR/GSK-3β Signalling Pathway to Improve Leptin Sensitivity and Alleviate Neuroinflammation in High-Fat Diet-Fed APP/PS1 Mice.Molecular neurobiology · 2025Article
- Modeling the emergence of viral resistance for SARS-CoV-2 during treatment with an anti-spike monoclonal antibody.PLoS pathogens · 2024Article
- Modeling the emergence of viral resistance for SARS-CoV-2 during treatment with an anti-spike monoclonal antibody.bioRxiv : the preprint server for biology · 2023Article
- Good and bad get together: Inactivation of SARS-CoV-2 in particulate matter pollution from different fuels.The Science of the total environment · 2022Article
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
- A small molecule compound berberine as an orally active therapeutic candidate against COVID-19 and SARS: A computational and mechanistic study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- ViralLink: An integrated workflow to investigate the effect of SARS-CoV-2 on intracellular signalling and regulatory pathways.PLoS computational biology · 2021Article
- Heparanase, cell signaling, and viral infections.Cellular and molecular life sciences : CMLS · 2020Review
- Mutations in the phosphorylation sites of SARS-CoV-2 encoded nucleocapsid protein and structure model of sequestration by protein 14-3-3.Biochemical and biophysical research communications · 2020Article
- Potential therapeutic targets and promising drugs for combating SARS-CoV-2.British journal of pharmacology · 2020Review
- COVID-19: viral-host interactome analyzed by network based-approach model to study pathogenesis of SARS-CoV-2 infection.Journal of translational medicine · 2020Article
- GSK-3 Inhibition as a Therapeutic Approach Against SARs CoV2: Dual Benefit of Inhibiting Viral Replication While Potentiating the Immune Response.Frontiers in immunology · 2020Review
- Magnetically enhanced nucleic acid delivery. Ten years of magnetofection-progress and prospects.Advanced drug delivery reviews · 2011Review
- Article
- Severe acute respiratory syndrome coronavirus evades antiviral signaling: role of nsp1 and rational design of an attenuated strain.Journal of virology · 2007Article
- The SARS-Coronavirus Membrane protein induces apoptosis through modulating the Akt survival pathway.Archives of biochemistry and biophysics · 2007Article
- Enhancement of cytotoxicity against Vero E6 cells persistently infected with SARS-CoV by Mycoplasma fermentans.Archives of virology · 2007Article
- Mechanisms of establishment of persistent SARS-CoV-infected cells.Biochemical and biophysical research communications · 2006Article
- Regulation of p90RSK phosphorylation by SARS-CoV infection in Vero E6 cells.FEBS letters · 2006Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome (SARS) is caused by SARS-coronavirus (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3beta, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3beta small interfering RNA indicated that the glycogen synthase kinase-3beta signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.
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