Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene.
Identifieur interne : 001F10 ( Ncbi/Merge ); précédent : 001F09; suivant : 001F11Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene.
Auteurs : Kam-Leung Siu ; Ching-Ping Chan ; Chris Chan ; Bo-Jian Zheng ; Dong-Yan JinSource :
- The Journal of general virology [ 0022-1317 ] ; 2009.
Descripteurs français
- KwdFr :
- Fibrinogène (génétique), Fibrinogène (métabolisme), Humains, Lignée cellulaire, Protéines nucléocapside (génétique), Protéines nucléocapside (métabolisme), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Transcription génétique, Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- génétique : Fibrinogène, Protéines nucléocapside, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Fibrinogène, Protéines nucléocapside, Syndrome respiratoire aigu sévère, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Humains, Lignée cellulaire, Transcription génétique.
English descriptors
- KwdEn :
- Cell Line, Fibrinogen (genetics), Fibrinogen (metabolism), Humans, Nucleocapsid Proteins (genetics), Nucleocapsid Proteins (metabolism), SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Transcription, Genetic.
- MESH :
- chemical , genetics : Fibrinogen, Nucleocapsid Proteins.
- chemical , metabolism : Fibrinogen, Nucleocapsid Proteins.
- genetics : SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Cell Line, Humans, Transcription, Genetic.
Abstract
Among the structural and nonstructural proteins of severe acute respiratory syndrome coronavirus (SARS-CoV), the nucleocapsid (N) protein plays pivotal roles in the biology and pathogenesis of viral infection. N protein is thought to dysregulate cell signalling and the transcription of cellular genes, including FGL2, which encodes a prothrombinase implicated in vascular thrombosis, fibrin deposition and pneumocyte necrosis. Here, we showed that N protein expressed in cultured human cells was predominantly found in the cytoplasm and was competent in repressing the transcriptional activity driven by interferon-stimulated response elements. However, the expression of N protein did not influence the transcription from the FGL2 promoter. More importantly, N protein did not modulate the expression of FGL2 mRNA or protein in transfected or SARS-CoV-infected cells. Taken together, our findings did not support the model in which SARS-CoV N protein specifically modulates transcription of the FGL2 gene to cause fibrosis and vascular thrombosis.
DOI: 10.1099/vir.0.009209-0
PubMed: 19423547
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pubmed:19423547Le document en format XML
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<author><name sortKey="Chan, Chris" sort="Chan, Chris" uniqKey="Chan C" first="Chris" last="Chan">Chris Chan</name>
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<author><name sortKey="Zheng, Bo Jian" sort="Zheng, Bo Jian" uniqKey="Zheng B" first="Bo-Jian" last="Zheng">Bo-Jian Zheng</name>
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<term>Nucleocapsid Proteins (genetics)</term>
<term>Nucleocapsid Proteins (metabolism)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (genetics)</term>
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<term>Fibrinogène (métabolisme)</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Protéines nucléocapside (génétique)</term>
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<term>Syndrome respiratoire aigu sévère (génétique)</term>
<term>Syndrome respiratoire aigu sévère (métabolisme)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Transcription génétique</term>
<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fibrinogen</term>
<term>Nucleocapsid Proteins</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Protéines nucléocapside</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Severe Acute Respiratory Syndrome</term>
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<term>Protéines nucléocapside</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virus du SRAS</term>
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<term>Humans</term>
<term>Transcription, Genetic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire</term>
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<front><div type="abstract" xml:lang="en">Among the structural and nonstructural proteins of severe acute respiratory syndrome coronavirus (SARS-CoV), the nucleocapsid (N) protein plays pivotal roles in the biology and pathogenesis of viral infection. N protein is thought to dysregulate cell signalling and the transcription of cellular genes, including FGL2, which encodes a prothrombinase implicated in vascular thrombosis, fibrin deposition and pneumocyte necrosis. Here, we showed that N protein expressed in cultured human cells was predominantly found in the cytoplasm and was competent in repressing the transcriptional activity driven by interferon-stimulated response elements. However, the expression of N protein did not influence the transcription from the FGL2 promoter. More importantly, N protein did not modulate the expression of FGL2 mRNA or protein in transfected or SARS-CoV-infected cells. Taken together, our findings did not support the model in which SARS-CoV N protein specifically modulates transcription of the FGL2 gene to cause fibrosis and vascular thrombosis.</div>
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<Abstract><AbstractText>Among the structural and nonstructural proteins of severe acute respiratory syndrome coronavirus (SARS-CoV), the nucleocapsid (N) protein plays pivotal roles in the biology and pathogenesis of viral infection. N protein is thought to dysregulate cell signalling and the transcription of cellular genes, including FGL2, which encodes a prothrombinase implicated in vascular thrombosis, fibrin deposition and pneumocyte necrosis. Here, we showed that N protein expressed in cultured human cells was predominantly found in the cytoplasm and was competent in repressing the transcriptional activity driven by interferon-stimulated response elements. However, the expression of N protein did not influence the transcription from the FGL2 promoter. More importantly, N protein did not modulate the expression of FGL2 mRNA or protein in transfected or SARS-CoV-infected cells. Taken together, our findings did not support the model in which SARS-CoV N protein specifically modulates transcription of the FGL2 gene to cause fibrosis and vascular thrombosis.</AbstractText>
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<name sortKey="Chan, Chris" sort="Chan, Chris" uniqKey="Chan C" first="Chris" last="Chan">Chris Chan</name>
<name sortKey="Jin, Dong Yan" sort="Jin, Dong Yan" uniqKey="Jin D" first="Dong-Yan" last="Jin">Dong-Yan Jin</name>
<name sortKey="Siu, Kam Leung" sort="Siu, Kam Leung" uniqKey="Siu K" first="Kam-Leung" last="Siu">Kam-Leung Siu</name>
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