Mechanisms of establishment of persistent SARS-CoV-infected cells
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Summary
Results indicated that at least four proteins, Akt, JNK, Bcl-2 and Bcl-2 and Bcl-xL, are necessary for survival of persistently SARS-CoV-infected cells.
- Type
- article
- Published
- 2006-06-22
- Cited by
- 35
- References
- 15
- Access
- Open access
- OpenAlex
- https://openalex.org/W2019312368
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:32868165
Keywords
Protein kinase B, PI3K/AKT/mTOR pathway, Phosphorylation, Vero cell, Biology
References
- Severe acute respiratory syndrome coronavirus persistence in Vero cells.
- JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells
- Spectrophotometric quantitation of anchorage-dependent cell numbers using extraction of naphthol blue-black-stained cellular protein.
- Regulation of p90RSK phosphorylation by SARS‐CoV infection in Vero E6 cells
- Establishment of Vero E6 cell clones persistently infected with severe acute respiratory syndrome coronavirus
- The SARS coronavirus nucleocapsid protein induces actin reorganization and apoptosis in COS-1 cells in the absence of growth factors.
- Inhibition of cell proliferation by SARS‐CoV infection in Vero E6 cells
- Persistent infection of SARS coronavirus in colonic cells in vitro
- Unknotting the roles of Bcl-2 and Bcl-xL in cell death.
- Induction of protective immunity against severe acute respiratory syndrome coronavirus (SARS-CoV) infection using highly attenuated recombinant vaccinia virus DIs
- Importance of Akt signaling pathway for apoptosis in SARS-CoV-infected Vero E6 cells
- Phosphorylation of p38 MAPK and its downstream targets in SARS coronavirus-infected cells
- Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome
- Tyrosine dephosphorylation of STAT3 in SARS coronavirus‐infected Vero E6 cells
- The Genome Sequence of the SARS-Associated Coronavirus
Cited by
- Investigation of the rescue of the rubella virus P150 replicase protein Q domain by the capsid protein
- Influenza A viruses and PI3K signalling
- MOLECULAR AND GENOMIC APPROACHES TO UNDERSTANDING HOST-VIRUS INTERACTIONS IN SHAPING THE OUTCOME OF EQUINE ARTERITIS VIRUS INFECTION
- From virus entry to release: the diverse functions of PI3K during RNA virus infections
- Cell Type-Specific Cleavage of Nucleocapsid Protein by Effector Caspases during SARS Coronavirus Infection
- Enhancement of cytotoxicity against Vero E6 cells persistently infected with SARS-CoV by Mycoplasma fermentans
- Smallpox Vaccines for Biodefense
- Persistent Equine Arteritis Virus Infection in HeLa Cells
- Magnetically enhanced nucleic acid delivery. Ten years of magnetofection—Progress and prospects
- A Network Integration Approach to Predict Conserved Regulators Related to Pathogenicity of Influenza and SARS-CoV Respiratory Viruses
- Triggering of DC migration by dengue virus stimulation of COX‐2‐dependent signaling cascades in vitro highlights the significance of these cascades beyond inflammation
- Proteomics Analysis Unravels the Functional Repertoire of Coronavirus Nonstructural Protein 3
- Quantitative Proteomics Analysis Reveals BAG3 as a Potential Target To Suppress Severe Acute Respiratory Syndrome Coronavirus Replication
- Regulation of Stress Responses and Translational Control by Coronavirus
- Molecular biology of the SARS-coronavirus
- The NF-κB-dependent and -independent transcriptome and chromatin landscapes of human coronavirus 229E-infected cells
- Activation of the c-Jun NH2-terminal kinase pathway by coronavirus infectious bronchitis virus promotes apoptosis independently of c-Jun
- Double-stranded viral RNA persists in vitro and in vivo during prolonged infection of porcine reproductive and respiratory syndrome virus.
- White-nose syndrome is associated with increased replication of a naturally persisting coronaviruses in bats
- The Alterations of Cellular Signaling Pathways in the Host Cell upon the High Pathogenic Coronaviruses Infection, SARS-CoV and MERS-CoV. What Could Be Expected from the SARS-CoV-2?
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