ArticleFEBS letters2004
Tyrosine dephosphorylation of STAT3 in SARS coronavirus-infected Vero E6 cells.
Article in FEBS letters, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 95 citations in OpenAlex.
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- Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective.The EMBO journal · 2024Review
- TheiScience · 2023Article
- A network-biology led computational drug repurposing strategy to prioritize therapeutic options for COVID-19.Heliyon · 2022Article
- Inhibition of the IFN-α JAK/STAT Pathway by MERS-CoV and SARS-CoV-1 Proteins in Human Epithelial Cells.Viruses · 2022Article
- A pathway map of signaling events triggered upon SARS-CoV infection.Journal of cell communication and signaling · 2021Article
- Article
- COVID-19 and cardiovascular diseases.Journal of molecular cell biology · 2021Review
- Contribution of STAT3 to the pathogenesis of COVID-19.Microbial pathogenesis · 2021Review
- Differential Signaling and Virus Production in Calu-3 Cells and Vero Cells upon SARS-CoV-2 Infection.Biomolecules & therapeutics · 2021Article
- Comorbidities and Susceptibility to COVID-19: A Generalized Gene Set Data Mining Approach.Journal of clinical medicine · 2021Article
- Article
- An Overview of Current Knowledge of Deadly CoVs and Their Interface with Innate Immunity.Viruses · 2021Review
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- The roles of signaling pathways in SARS-CoV-2 infection; lessons learned from SARS-CoV and MERS-CoV.Archives of virology · 2021Review
- Upregulation of DUSP6 impairs infectious bronchitis virus replication by negatively regulating ERK pathway and promoting apoptosis.Veterinary research · 2021Article
- The Many Faces of JAKs and STATs Within the COVID-19 Storm.Frontiers in immunology · 2021Review
- Translational control of coronaviruses.Nucleic acids research · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome (SARS) has become a global public health emergency. p38 mitogen-activated protein kinase (MAPK) and its downstream targets are activated in SARS coronavirus (SARS-CoV)-infected Vero E6 cells and activation of p38 MAPK enhances the cytopathic effects of SARS-CoV infection. In addition, weak activation of Akt cannot prevent SARS-CoV infection-induced apoptosis in Vero E6 cells. In the present study, we demonstrated that signal transducer and activator of transcription (STAT) 3, which is constitutively phosphorylated at tyrosine (Tyr)-705 and slightly phosphorylated at serine (Ser)-727 in Vero E6 cells, was dephosphorylated at Tyr-705 on SARS-CoV infection. In addition to phosphorylation of p38 MAPK in virus-infected cells, other MAPKs, i.e., extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK), were phosphorylated. Although inhibitors of ERK1/2 and JNK (PD98059 and SP600125) had no effect on phosphorylation status of STAT3, inhibitors of p38 MAPK (SB203580 and SB202190) partially inhibited dephosphorylation of STAT3 at Tyr-705. Tyr-705-phosphorylated STAT3 was localized mainly in the nucleus in mock infected cells, whereas STAT3 disappeared from the nucleus in virus-infected cells. As STAT3 acts as an activator of transcription in the nucleus, these results suggest that STAT3 lacks its activity on transcription in SARS-CoV-infected Vero E6 cells.
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