SARS-CoV accessory protein 3b induces AP-1 transcriptional activity through activation of JNK and ERK pathways.
Identifieur interne : 002336 ( Ncbi/Curation ); précédent : 002335; suivant : 002337SARS-CoV accessory protein 3b induces AP-1 transcriptional activity through activation of JNK and ERK pathways.
Auteurs : Bhavna Varshney [Inde] ; Sunil K. LalSource :
- Biochemistry [ 1520-4995 ] ; 2011.
Descripteurs français
- KwdFr :
- Activation de la transcription, Animaux, Cellules Vero, Chimiokine CCL2 (génétique), Facteur de transcription AP-1 (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Humains, JNK Mitogen-Activated Protein Kinases (métabolisme), Lignée cellulaire, Protéines proto-oncogènes c-fos (métabolisme), Protéines recombinantes (génétique), Protéines recombinantes (métabolisme), Protéines virales régulatrices ou accessoires (génétique), Protéines virales régulatrices ou accessoires (métabolisme), Régions promotrices (génétique), Sondes d'ADN (génétique), Système de signalisation des MAP kinases, Séquence nucléotidique, Transduction du signal, Transfection, Virulence, Virus du SRAS (génétique), Virus du SRAS (métabolisme), Virus du SRAS (pathogénicité).
- MESH :
- génétique : Chimiokine CCL2, Protéines recombinantes, Protéines virales régulatrices ou accessoires, Sondes d'ADN, Virus du SRAS.
- métabolisme : Facteur de transcription AP-1, Facteur-3 de régulation d'interféron, JNK Mitogen-Activated Protein Kinases, Protéines proto-oncogènes c-fos, Protéines recombinantes, Protéines virales régulatrices ou accessoires, Virus du SRAS.
- pathogénicité : Virus du SRAS.
- Activation de la transcription, Animaux, Cellules Vero, Humains, Lignée cellulaire, Régions promotrices (génétique), Système de signalisation des MAP kinases, Séquence nucléotidique, Transduction du signal, Transfection, Virulence.
English descriptors
- KwdEn :
- Animals, Base Sequence, Cell Line, Chemokine CCL2 (genetics), Chlorocebus aethiops, DNA Probes (genetics), Humans, Interferon Regulatory Factor-3 (metabolism), JNK Mitogen-Activated Protein Kinases (metabolism), MAP Kinase Signaling System, Promoter Regions, Genetic, Proto-Oncogene Proteins c-fos (metabolism), Recombinant Proteins (genetics), Recombinant Proteins (metabolism), SARS Virus (genetics), SARS Virus (metabolism), SARS Virus (pathogenicity), Signal Transduction, Transcription Factor AP-1 (metabolism), Transcriptional Activation, Transfection, Vero Cells, Viral Regulatory and Accessory Proteins (genetics), Viral Regulatory and Accessory Proteins (metabolism), Virulence.
- MESH :
- chemical , genetics : Chemokine CCL2, DNA Probes, Recombinant Proteins, Viral Regulatory and Accessory Proteins.
- chemical , metabolism : Interferon Regulatory Factor-3, JNK Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-fos, Recombinant Proteins, Transcription Factor AP-1, Viral Regulatory and Accessory Proteins.
- genetics : SARS Virus.
- metabolism : SARS Virus.
- pathogenicity : SARS Virus.
- Animals, Base Sequence, Cell Line, Chlorocebus aethiops, Humans, MAP Kinase Signaling System, Promoter Regions, Genetic, Signal Transduction, Transcriptional Activation, Transfection, Vero Cells, Virulence.
Abstract
The outbreak of severe acute respiratory syndrome (SARS) in 2003 in China, characterized by atypical pneumonia, was associated with the emergence of a novel coronavirus named severe acute respiratory syndrome coronavirus (SARS-CoV). Eight accessory proteins of SARS coronavirus were the suspected players in the pathogenesis of the virus. Among them, protein 3b localizes to the nucleus and behaves as an interferon antagonist by inhibiting IRF3 activation. However, the effect of 3b on the activity of other common host transcription factors remains unexplored. In this work, we studied the effect of 3b on the transcriptional activity of AP-1. Our findings elucidate augmentation of AP-1-dependent gene expression in 3b-transfected Huh7 cells. Reporter gene and mobility shift assays depict an increase in the AP-1 transcriptional and DNA binding activity in the presence of 3b. This increase in activity correlates with the activation of ERK and JNK pathways. Furthermore, 3b expression potentiates AP-1-driven promoter activity of proinflammatory cytokine MCP-1, suggesting a plausible role for 3b as a virulence factor that might function by upregulating AP-1-dependent cytokine levels in SARS-CoV infection.
DOI: 10.1021/bi200303r
PubMed: 21561061
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(metabolism)</term><term>Transcriptional Activation</term><term>Transfection</term><term>Vero Cells</term><term>Viral Regulatory and Accessory Proteins (genetics)</term><term>Viral Regulatory and Accessory Proteins (metabolism)</term><term>Virulence</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation de la transcription</term><term>Animaux</term><term>Cellules Vero</term><term>Chimiokine CCL2 (génétique)</term><term>Facteur de transcription AP-1 (métabolisme)</term><term>Facteur-3 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term><term>Lignée cellulaire</term><term>Protéines proto-oncogènes c-fos (métabolisme)</term><term>Protéines recombinantes (génétique)</term><term>Protéines recombinantes (métabolisme)</term><term>Protéines virales régulatrices ou accessoires (génétique)</term><term>Protéines virales régulatrices ou accessoires (métabolisme)</term><term>Régions promotrices (génétique)</term><term>Sondes d'ADN (génétique)</term><term>Système de signalisation des MAP kinases</term><term>Séquence nucléotidique</term><term>Transduction du signal</term><term>Transfection</term><term>Virulence</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (métabolisme)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chemokine CCL2</term><term>DNA Probes</term><term>Recombinant Proteins</term><term>Viral Regulatory and Accessory Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interferon Regulatory Factor-3</term><term>JNK Mitogen-Activated Protein Kinases</term><term>Proto-Oncogene Proteins c-fos</term><term>Recombinant Proteins</term><term>Transcription Factor AP-1</term><term>Viral Regulatory and Accessory Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Chimiokine CCL2</term><term>Protéines recombinantes</term><term>Protéines virales régulatrices ou accessoires</term><term>Sondes d'ADN</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription AP-1</term><term>Facteur-3 de régulation d'interféron</term><term>JNK Mitogen-Activated Protein Kinases</term><term>Protéines proto-oncogènes c-fos</term><term>Protéines recombinantes</term><term>Protéines virales régulatrices ou accessoires</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Cell Line</term><term>Chlorocebus aethiops</term><term>Humans</term><term>MAP Kinase Signaling System</term><term>Promoter Regions, Genetic</term><term>Signal Transduction</term><term>Transcriptional Activation</term><term>Transfection</term><term>Vero Cells</term><term>Virulence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation de la transcription</term><term>Animaux</term><term>Cellules Vero</term><term>Humains</term><term>Lignée cellulaire</term><term>Régions promotrices (génétique)</term><term>Système de signalisation des MAP kinases</term><term>Séquence nucléotidique</term><term>Transduction du signal</term><term>Transfection</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The outbreak of severe acute respiratory syndrome (SARS) in 2003 in China, characterized by atypical pneumonia, was associated with the emergence of a novel coronavirus named severe acute respiratory syndrome coronavirus (SARS-CoV). Eight accessory proteins of SARS coronavirus were the suspected players in the pathogenesis of the virus. Among them, protein 3b localizes to the nucleus and behaves as an interferon antagonist by inhibiting IRF3 activation. However, the effect of 3b on the activity of other common host transcription factors remains unexplored. In this work, we studied the effect of 3b on the transcriptional activity of AP-1. Our findings elucidate augmentation of AP-1-dependent gene expression in 3b-transfected Huh7 cells. Reporter gene and mobility shift assays depict an increase in the AP-1 transcriptional and DNA binding activity in the presence of 3b. This increase in activity correlates with the activation of ERK and JNK pathways. Furthermore, 3b expression potentiates AP-1-driven promoter activity of proinflammatory cytokine MCP-1, suggesting a plausible role for 3b as a virulence factor that might function by upregulating AP-1-dependent cytokine levels in SARS-CoV infection.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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