The SARS coronavirus nucleocapsid protein induces actin reorganization and apoptosis in COS-1 cells in the absence of growth factors.
Identifieur interne : 002C36 ( PubMed/Curation ); précédent : 002C35; suivant : 002C37The SARS coronavirus nucleocapsid protein induces actin reorganization and apoptosis in COS-1 cells in the absence of growth factors.
Auteurs : Milan Surjit [Inde] ; Boping Liu ; Shahid Jameel ; Vincent T K. Chow ; Sunil K. LalSource :
- The Biochemical journal [ 1470-8728 ] ; 2004.
Descripteurs français
- KwdFr :
- Actines (métabolisme), Animaux, Apoptose (physiologie), Caspases (métabolisme), Cellules COS, Fibronectines (métabolisme), Focal adhesion protein-tyrosine kinases, Intégrines (physiologie), Lignée cellulaire tumorale, Milieux de culture sans sérum, Mitogen-Activated Protein Kinases (métabolisme), Protein-Serine-Threonine Kinases (métabolisme), Protein-tyrosine kinases (métabolisme), Protéines nucléocapside (physiologie), Protéines proto-oncogènes (métabolisme), Protéines proto-oncogènes c-akt, Régulation négative, Régulation positive, Substances de croissance (physiologie), Transfection, Virus du SRAS (physiologie).
- MESH :
- métabolisme : Actines, Caspases, Fibronectines, Mitogen-Activated Protein Kinases, Protein-Serine-Threonine Kinases, Protein-tyrosine kinases, Protéines proto-oncogènes.
- physiologie : Apoptose, Intégrines, Protéines nucléocapside, Substances de croissance, Virus du SRAS.
- Animaux, Cellules COS, Focal adhesion protein-tyrosine kinases, Lignée cellulaire tumorale, Milieux de culture sans sérum, Protéines proto-oncogènes c-akt, Régulation négative, Régulation positive, Transfection.
English descriptors
- KwdEn :
- Actins (metabolism), Animals, Apoptosis (physiology), COS Cells, Caspases (metabolism), Cell Line, Tumor, Chlorocebus aethiops, Culture Media, Serum-Free, Down-Regulation, Fibronectins (metabolism), Focal Adhesion Protein-Tyrosine Kinases, Growth Substances (physiology), Integrins (physiology), Mitogen-Activated Protein Kinases (metabolism), Nucleocapsid Proteins (physiology), Protein-Serine-Threonine Kinases (metabolism), Protein-Tyrosine Kinases (metabolism), Proto-Oncogene Proteins (metabolism), Proto-Oncogene Proteins c-akt, SARS Virus (physiology), Transfection, Up-Regulation.
- MESH :
- chemical , metabolism : Actins, Caspases, Fibronectins, Mitogen-Activated Protein Kinases, Protein-Serine-Threonine Kinases, Protein-Tyrosine Kinases, Proto-Oncogene Proteins.
- physiology : Apoptosis, Growth Substances, Integrins, Nucleocapsid Proteins, SARS Virus.
- Animals, COS Cells, Cell Line, Tumor, Chlorocebus aethiops, Culture Media, Serum-Free, Down-Regulation, Focal Adhesion Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-akt, Transfection, Up-Regulation.
Abstract
In March 2003, a novel coronavirus was isolated from patients exhibiting atypical pneumonia, and was subsequently proven to be the causative agent of the disease now referred to as SARS (severe acute respiratory syndrome). The complete genome of the SARS-CoV (SARS coronavirus) has since been sequenced. The SARS-CoV nucleocapsid (SARS-CoV N) protein shares little homology with other members of the coronavirus family. In the present paper, we show that SARS-CoV N is capable of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth factors by down-regulating ERK (extracellular-signal-regulated kinase), up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) pathways, and affecting their downstream effectors. SARS-CoV N expression also down-regulated phospho-Akt and Bcl-2 levels, and activated caspases 3 and 7. However, apoptosis was independent of the p53 and Fas signalling pathways. Furthermore, activation of the p38 MAPK pathway was found to induce actin reorganization in cells devoid of growth factors. At the cytoskeletal level, SARS-CoV N down-regulated FAK (focal adhesion kinase) activity and also down-regulated fibronectin expression. This is the first report showing the ability of the N protein of SARS-CoV to induce apoptosis and actin reorganization in mammalian cells under stressed conditions.
DOI: 10.1042/BJ20040984
PubMed: 15294014
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pubmed:15294014Le document en format XML
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<front><div type="abstract" xml:lang="en">In March 2003, a novel coronavirus was isolated from patients exhibiting atypical pneumonia, and was subsequently proven to be the causative agent of the disease now referred to as SARS (severe acute respiratory syndrome). The complete genome of the SARS-CoV (SARS coronavirus) has since been sequenced. The SARS-CoV nucleocapsid (SARS-CoV N) protein shares little homology with other members of the coronavirus family. In the present paper, we show that SARS-CoV N is capable of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth factors by down-regulating ERK (extracellular-signal-regulated kinase), up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) pathways, and affecting their downstream effectors. SARS-CoV N expression also down-regulated phospho-Akt and Bcl-2 levels, and activated caspases 3 and 7. However, apoptosis was independent of the p53 and Fas signalling pathways. Furthermore, activation of the p38 MAPK pathway was found to induce actin reorganization in cells devoid of growth factors. At the cytoskeletal level, SARS-CoV N down-regulated FAK (focal adhesion kinase) activity and also down-regulated fibronectin expression. This is the first report showing the ability of the N protein of SARS-CoV to induce apoptosis and actin reorganization in mammalian cells under stressed conditions.</div>
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<Abstract><AbstractText>In March 2003, a novel coronavirus was isolated from patients exhibiting atypical pneumonia, and was subsequently proven to be the causative agent of the disease now referred to as SARS (severe acute respiratory syndrome). The complete genome of the SARS-CoV (SARS coronavirus) has since been sequenced. The SARS-CoV nucleocapsid (SARS-CoV N) protein shares little homology with other members of the coronavirus family. In the present paper, we show that SARS-CoV N is capable of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth factors by down-regulating ERK (extracellular-signal-regulated kinase), up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase) pathways, and affecting their downstream effectors. SARS-CoV N expression also down-regulated phospho-Akt and Bcl-2 levels, and activated caspases 3 and 7. However, apoptosis was independent of the p53 and Fas signalling pathways. Furthermore, activation of the p38 MAPK pathway was found to induce actin reorganization in cells devoid of growth factors. At the cytoskeletal level, SARS-CoV N down-regulated FAK (focal adhesion kinase) activity and also down-regulated fibronectin expression. This is the first report showing the ability of the N protein of SARS-CoV to induce apoptosis and actin reorganization in mammalian cells under stressed conditions.</AbstractText>
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