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 : 000371Proteomic 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 LinSource :
- Proteomics : (Weinheim. Print) [ 1615-9853 ] ; 2007.
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- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 07-0263474 INIST |
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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 |
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Pascal:07-0263474Le 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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<s5>08</s5>
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<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>
</standard>
<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>
</server>
</inist>
</record>
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