SrasV1, PascalFrancis, Corpus, bibRecord, 000516

Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis

Identifieur interne : 000516 ( PascalFrancis/Corpus ); précédent : 000515; suivant : 000517

Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis

Auteurs : Cheng-Wen Lin ; Kuan-Hsun Lin ; Tsung-Han Hsieh ; Shi-Yi Shiu ; Jeng-Yi Li

Source :

FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.

RBID : Pascal:06-0198935

Descripteurs français

Pascal (Inist)
- Coronavirus, Virus syndrome respiratoire aigu sévère, Peptidases, Apoptose, Mort cellulaire, Microbiologie, Immunologie, Syndrome respiratoire aigu sévère, Oxygène actif.

English descriptors

KwdEn :
- Apoptosis, Cell death, Coronavirus, Immunology, Microbiology, Peptidases, Severe acute respiratory syndrome, Severe acute respiratory syndrome virus.

Abstract

The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL^pro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL^pro-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL^pro-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL^pro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 LIN (Cheng-Wen)`
A11	`02`	`1`		`@1 LIN (Kuan-Hsun)`
A11	`03`	`1`		`@1 HSIEH (Tsung-Han)`
A11	`04`	`1`		`@1 SHIU (Shi-Yi)`
A11	`05`	`1`		`@1 LI (Jeng-Yi)`
A14	`01`			`@1 Department of Medical Laboratory Science and Biotechnology, China Medical University @2 Taichung @3 TWN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut.`
A14	`02`			`@1 Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital @2 Taichung @3 TWN @Z 1 aut.`
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A21				`@1 2006`
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A43	`01`			`@1 INIST @2 17567B @5 354000132467810080`
A44				`@0 0000 @1 © 2006 INIST-CNRS. All rights reserved.`
A45				`@0 27 ref.`
A47	`01`	`1`		`@0 06-0198935`
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A64	`01`	`1`		`@0 FEMS immunology and medical microbiology`
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C01	`01`		`ENG`	@0 The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL^pro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL^pro-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL^pro-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL^pro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.
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C07	`07`	`X`	`FRE`	`@0 Virose`
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Format Inist (serveur)

NO :	PASCAL 06-0198935 INIST
ET :	Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis
AU :	LIN (Cheng-Wen); LIN (Kuan-Hsun); HSIEH (Tsung-Han); SHIU (Shi-Yi); LI (Jeng-Yi)
AF :	Department of Medical Laboratory Science and Biotechnology, China Medical University/Taichung/Taïwan (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital/Taichung/Taïwan (1 aut.)
DT :	Publication en série; Niveau analytique
SO :	FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2006; Vol. 46; No. 3; Pp. 375-380; Bibl. 27 ref.
LA :	Anglais
EA :	The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL^pro) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL^pro-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL^pro-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL^pro increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.
CC :	002A05C10
FD :	Coronavirus; Virus syndrome respiratoire aigu sévère; Peptidases; Apoptose; Mort cellulaire; Microbiologie; Immunologie; Syndrome respiratoire aigu sévère; Oxygène actif
FG :	Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED :	Coronavirus; Severe acute respiratory syndrome virus; Peptidases; Apoptosis; Cell death; Microbiology; Immunology; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Coronavirus; Severe acute respiratory syndrome virus; Peptidases; Apoptosis; Muerte celular; Microbiología; Inmunología; Síndrome respiratorio agudo severo
LO :	INIST-17567B.354000132467810080
ID :	06-0198935

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Pascal:06-0198935

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<front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL<sup>pro</sup>
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-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL<sup>pro</sup>
-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL<sup>pro</sup>
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<fC01 i1="01" l="ENG"><s0>The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL<sup>pro</sup>
) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL<sup>pro</sup>
-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL<sup>pro</sup>
-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL<sup>pro</sup>
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</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>05</s5>
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<fC03 i1="03" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>05</s5>
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<fC03 i1="03" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>05</s5>
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<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Apoptosis</s0>
<s5>06</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Apoptosis</s0>
<s5>06</s5>
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<s5>07</s5>
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<s5>07</s5>
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<s5>14</s5>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>FE</s2>
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<s2>FE</s2>
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<s2>FE</s2>
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<s2>FE</s2>
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<fC07 i1="05" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
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<s2>FE</s2>
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<s5>13</s5>
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<fC07 i1="06" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
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<s5>13</s5>
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<fC07 i1="08" i2="X" l="SPA"><s0>Infección</s0>
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<fC07 i1="09" i2="X" l="FRE"><s0>Poumon pathologie</s0>
<s5>16</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>16</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>16</s5>
</fC07>
<fN21><s1>128</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 06-0198935 INIST</NO>
<ET>Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis</ET>
<AU>LIN (Cheng-Wen); LIN (Kuan-Hsun); HSIEH (Tsung-Han); SHIU (Shi-Yi); LI (Jeng-Yi)</AU>
<AF>Department of Medical Laboratory Science and Biotechnology, China Medical University/Taichung/Taïwan (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital/Taichung/Taïwan (1 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2006; Vol. 46; No. 3; Pp. 375-380; Bibl. 27 ref.</SO>
<LA>Anglais</LA>
<EA>The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS-CoV has been demonstrated to induce cell apoptosis in Vero-E6 cells. The possible role of SARS-CoV 3C-like protease (3CL<sup>pro</sup>
) in virus-induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase-3 and caspase-9 activities were demonstrated in SARS-CoV 3CL<sup>pro</sup>
-expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS-CoV 3CL<sup>pro</sup>
-expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL<sup>pro</sup>
 increased the activation of the nuclear factor-kappa B-dependent reporter, but inhibited activator protein-1-dependent transcription. This finding is likely to be responsible for virus-induced apoptotic signalling.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Virus syndrome respiratoire aigu sévère; Peptidases; Apoptose; Mort cellulaire; Microbiologie; Immunologie; Syndrome respiratoire aigu sévère; Oxygène actif</FD>
<FG>Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Coronavirus; Severe acute respiratory syndrome virus; Peptidases; Apoptosis; Cell death; Microbiology; Immunology; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Severe acute respiratory syndrome virus; Peptidases; Apoptosis; Muerte celular; Microbiología; Inmunología; Síndrome respiratorio agudo severo</SD>
<LO>INIST-17567B.354000132467810080</LO>
<ID>06-0198935</ID>
</server>
</inist>
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Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis

Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis

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