Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene
Identifieur interne : 002F07 ( Main/Exploration ); précédent : 002F06; suivant : 002F08Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene
Auteurs : Kam-Leung Siu [Hong Kong] ; Ching-Ping Chan [Hong Kong] ; Chris Chan [Hong Kong] ; Bo-Jian Zheng [Hong Kong] ; Dong-Yan Jin [Hong Kong]Source :
- 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.
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Cell Line, Coronavirus, Fibrinogen (genetics), Fibrinogen (metabolism), Gene, Human, Humans, Microbiology, Nucleocapsid, Nucleocapsid Proteins (genetics), Nucleocapsid Proteins (metabolism), Protein, SARS Virus (genetics), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Severe acute respiratory syndrome, Transcription, 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.
Affiliations:
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<term>Coronavirus</term>
<term>Fibrinogen (genetics)</term>
<term>Fibrinogen (metabolism)</term>
<term>Gene</term>
<term>Human</term>
<term>Humans</term>
<term>Microbiology</term>
<term>Nucleocapsid</term>
<term>Nucleocapsid Proteins (genetics)</term>
<term>Nucleocapsid Proteins (metabolism)</term>
<term>Protein</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (genetics)</term>
<term>Severe Acute Respiratory Syndrome (metabolism)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Severe acute respiratory syndrome</term>
<term>Transcription</term>
<term>Transcription, Genetic</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Fibrinogène (génétique)</term>
<term>Fibrinogène (métabolisme)</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Protéines nucléocapside (génétique)</term>
<term>Protéines nucléocapside (métabolisme)</term>
<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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<term>Nucleocapsid Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fibrinogen</term>
<term>Nucleocapsid Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Fibrinogène</term>
<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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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
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<term>Transcription, Genetic</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>
</front>
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<name sortKey="Chan, Ching Ping" sort="Chan, Ching Ping" uniqKey="Chan C" first="Ching-Ping" last="Chan">Ching-Ping Chan</name>
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