SrasV1, PascalFrancis, Corpus, bibRecord, 000370

Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease

Identifieur interne : 000370 ( PascalFrancis/Corpus ); précédent : 000369; suivant : 000371

Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease

Auteurs : Chien-Chen Lail ; Ming-Jia Jou ; Shiuan-Yi Huang ; Shih-Wein Li ; Lei Want ; Fuu-Jen Tsai ; Cheng-Wen Lin

Source :

Proteomics : (Weinheim. Print) [ 1615-9853 ] ; 2007.

RBID : Pascal:07-0263474

Descripteurs français

Pascal (Inist)
- Homme, Coronavirus, Virus syndrome respiratoire aigu sévère, Protéomique, Régulation, Protéine, Peptidases, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Coronavirus, Human, Peptidases, Protein, Proteomics, Regulation(control), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus.

Abstract

The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.
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Format Inist (serveur)

NO :	PASCAL 07-0263474 INIST
ET :	Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease
AU :	LAIL (Chien-Chen); JOU (Ming-Jia); HUANG (Shiuan-Yi); LI (Shih-Wein); WANT (Lei); TSAI (Fuu-Jen); LIN (Cheng-Wen)
AF :	Department of Medical Genetics and Medical Research, China Medical University Hospital/Taichung/Taïwan (1 aut., 3 aut., 5 aut., 6 aut.); Institute of Molecular Biology, National Chung Hsing University/Taichung/Taïwan (1 aut.); Department of Anatomy, School of Medicine, China Medical University/Taichung/Taïwan (2 aut.); Department of Medical Laboratory Science and Biotechnology, China Medical University/Taichung/Taïwan (4 aut., 7 aut.); Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital/Taichung/Taïwan (7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Proteomics : (Weinheim. Print); ISSN 1615-9853; Allemagne; Da. 2007; Vol. 7; No. 9; Pp. 1446-1460; Bibl. 42 ref.
LA :	Anglais
EA :	The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.
CC :	002A02D10; 002B05C02C
FD :	Homme; Coronavirus; Virus syndrome respiratoire aigu sévère; Protéomique; Régulation; Protéine; Peptidases; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie
ED :	Human; Coronavirus; Severe acute respiratory syndrome virus; Proteomics; Regulation(control); Protein; Peptidases; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Hombre; Coronavirus; Severe acute respiratory syndrome virus; Proteómica; Regulación; Proteína; Peptidases; Síndrome respiratorio agudo severo
LO :	INIST-27206.354000149448550080
ID :	07-0263474

Links to Exploration step

Pascal:07-0263474

Le document en format XML

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<front><div type="abstract" xml:lang="en">The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.</div>
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<fA03 i2="1"><s0>Proteomics : (Weinh., Print)</s0>
</fA03>
<fA05><s2>7</s2>
</fA05>
<fA06><s2>9</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>LAIL (Chien-Chen)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>JOU (Ming-Jia)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>HUANG (Shiuan-Yi)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>LI (Shih-Wein)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>WANT (Lei)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>TSAI (Fuu-Jen)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>LIN (Cheng-Wen)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Medical Genetics and Medical Research, China Medical University Hospital</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Institute of Molecular Biology, National Chung Hsing University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Anatomy, School of Medicine, China Medical University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Medical Laboratory Science and Biotechnology, China Medical University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>1446-1460</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>27206</s2>
<s5>354000149448550080</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2007 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>42 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>07-0263474</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Proteomics : (Weinheim. Print)</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A02D10</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05C02C</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Homme</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Human</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Hombre</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Virus syndrome respiratoire aigu sévère</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Severe acute respiratory syndrome virus</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Protéomique</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Proteomics</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Proteómica</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Régulation</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Regulation(control)</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Regulación</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Protéine</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Protein</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Proteína</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<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>176</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 07-0263474 INIST</NO>
<ET>Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease</ET>
<AU>LAIL (Chien-Chen); JOU (Ming-Jia); HUANG (Shiuan-Yi); LI (Shih-Wein); WANT (Lei); TSAI (Fuu-Jen); LIN (Cheng-Wen)</AU>
<AF>Department of Medical Genetics and Medical Research, China Medical University Hospital/Taichung/Taïwan (1 aut., 3 aut., 5 aut., 6 aut.); Institute of Molecular Biology, National Chung Hsing University/Taichung/Taïwan (1 aut.); Department of Anatomy, School of Medicine, China Medical University/Taichung/Taïwan (2 aut.); Department of Medical Laboratory Science and Biotechnology, China Medical University/Taichung/Taïwan (4 aut., 7 aut.); Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital/Taichung/Taïwan (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Proteomics : (Weinheim. Print); ISSN 1615-9853; Allemagne; Da. 2007; Vol. 7; No. 9; Pp. 1446-1460; Bibl. 42 ref.</SO>
<LA>Anglais</LA>
<EA>The pathogenesis of severe acute respiratory syndrome coronavirus (SARS CoV) is an important issue for treatment and prevention of SARS. Previously, SARS CoV 3C-like protease (3CLpro) has been demonstrated to induce apoptosis via the activation of caspase-3 and caspase-9 (Lin, C. W., Lin, K. H., Hsieh, T. H., Shiu, S. Y. et al., FEMS Immunol. Med. Microbiol. 2006, 46, 375-380). In this study, proteome analysis of the human promonocyte HL-CZ cells expressing SARS CoV 3CLpro was performed using 2-DE and nanoscale capillary LC/ESI quadrupole-TOF MS. Functional classification of identified up-regulated proteins indicated that protein metabolism and modification, particularly in the ubiquitin proteasome pathway, was the main biological process occurring in SARS CoV 3CLpro-expressing cells. Thirty-six percent of identified up-regulated proteins were located in the mitochondria, including apoptosis-inducing factor, ATP synthase beta chain and cytochrome c oxidase. Interestingly, heat shock cognate 71-kDa protein (HSP70), which antagonizes apoptosis-inducing factor was shown to down-regulate and had a 5.29-fold decrease. In addition, confocal image analysis has shown release of mitochondrial apoptogenic apoptosis-inducing factor and cytochrome c into the cytosol. Our results revealed that SARS CoV 3CLpro could be considered to induce mitochondrial-mediated apoptosis. The study provides system-level insights into the interaction of SARS CoV 3CLpro with host cells, which will be helpful in elucidating the molecular basis of SARS CoV pathogenesis.</EA>
<CC>002A02D10; 002B05C02C</CC>
<FD>Homme; Coronavirus; Virus syndrome respiratoire aigu sévère; Protéomique; Régulation; Protéine; Peptidases; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG>
<ED>Human; Coronavirus; Severe acute respiratory syndrome virus; Proteomics; Regulation(control); Protein; Peptidases; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Hombre; Coronavirus; Severe acute respiratory syndrome virus; Proteómica; Regulación; Proteína; Peptidases; Síndrome respiratorio agudo severo</SD>
<LO>INIST-27206.354000149448550080</LO>
<ID>07-0263474</ID>
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Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease

Proteomic analysis of up-regulated proteins in human promonocyte cells expressing severe acute respiratory syndrome coronavirus 3C-like protease

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