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Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene

Identifieur interne : 000191 ( PascalFrancis/Corpus ); précédent : 000190; suivant : 000192

Severe 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 Jin

Source :

RBID : Pascal:09-0375283

Descripteurs français

English descriptors

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0022-1317
A02 01      @0 JGVIAY
A03   1    @0 J. gen. virol.
A05       @2 90
A06       @3 p. 9
A08 01  1  ENG  @1 Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene
A11 01  1    @1 SIU (Kam-Leung)
A11 02  1    @1 CHAN (Ching-Ping)
A11 03  1    @1 CHAN (Chris)
A11 04  1    @1 ZHENG (Bo-Jian)
A11 05  1    @1 JIN (Dong-Yan)
A14 01      @1 Department of Biochemistry, Faculty of Medicine, The University of Hong Kong @3 HKG @Z 1 aut. @Z 2 aut. @Z 5 aut.
A14 02      @1 Department of Microbiology, Faculty of Medicine, The University of Hong Kong @3 HKG @Z 3 aut. @Z 4 aut.
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A23 01      @0 ENG
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A44       @0 0000 @1 © 2009 INIST-CNRS. All rights reserved.
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A47 01  1    @0 09-0375283
A60       @1 P @3 CC
A61       @0 A
A64 01  1    @0 Journal of general virology
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C01 01    ENG  @0 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.
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C07 01  X  ENG  @0 Coronaviridae @2 NW
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C07 04  X  SPA  @0 Aparato respiratorio patología @5 13
C07 05  X  FRE  @0 Virose
C07 05  X  ENG  @0 Viral disease
C07 05  X  SPA  @0 Virosis
C07 06  X  FRE  @0 Infection
C07 06  X  ENG  @0 Infection
C07 06  X  SPA  @0 Infección
C07 07  X  FRE  @0 Pathologie des poumons @5 16
C07 07  X  ENG  @0 Lung disease @5 16
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N21       @1 271
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Format Inist (serveur)

NO : PASCAL 09-0375283 INIST
ET : Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene
AU : SIU (Kam-Leung); CHAN (Ching-Ping); CHAN (Chris); ZHENG (Bo-Jian); JIN (Dong-Yan)
AF : Department of Biochemistry, Faculty of Medicine, The University of Hong Kong/Hong-Kong (1 aut., 2 aut., 5 aut.); Department of Microbiology, Faculty of Medicine, The University of Hong Kong/Hong-Kong (3 aut., 4 aut.)
DT : Publication en série; Courte communication, note brève; Niveau analytique
SO : Journal of general virology; ISSN 0022-1317; Coden JGVIAY; Royaume-Uni; Da. 2009; Vol. 90; No. p. 9; Pp. 2107-2113; Bibl. 1 p.3/4
LA : Anglais
EA : 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.
CC : 002A05C10
FD : Coronavirus; Homme; Nucléocapside; Protéine; Transcription; Gène; Microbiologie; Syndrome respiratoire aigu sévère
FG : Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons
ED : Coronavirus; Human; Nucleocapsid; Protein; Transcription; Gene; Microbiology; Severe acute respiratory syndrome
EG : Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease
SD : Coronavirus; Hombre; Nucleocápside; Proteína; Transcripción; Gen; Microbiología; Síndrome respiratorio agudo severo
LO : INIST-13533.354000171854490060
ID : 09-0375283

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Pascal:09-0375283

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<NO>PASCAL 09-0375283 INIST</NO>
<ET>Severe acute respiratory syndrome coronavirus nucleocapsid protein does not modulate transcription of the human FGL2 gene</ET>
<AU>SIU (Kam-Leung); CHAN (Ching-Ping); CHAN (Chris); ZHENG (Bo-Jian); JIN (Dong-Yan)</AU>
<AF>Department of Biochemistry, Faculty of Medicine, The University of Hong Kong/Hong-Kong (1 aut., 2 aut., 5 aut.); Department of Microbiology, Faculty of Medicine, The University of Hong Kong/Hong-Kong (3 aut., 4 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Journal of general virology; ISSN 0022-1317; Coden JGVIAY; Royaume-Uni; Da. 2009; Vol. 90; No. p. 9; Pp. 2107-2113; Bibl. 1 p.3/4</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Homme; Nucléocapside; Protéine; Transcription; Gène; Microbiologie; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons</FG>
<ED>Coronavirus; Human; Nucleocapsid; Protein; Transcription; Gene; Microbiology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Hombre; Nucleocápside; Proteína; Transcripción; Gen; Microbiología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13533.354000171854490060</LO>
<ID>09-0375283</ID>
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