Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.
Identifieur interne : 006738 ( Main/Exploration ); précédent : 006737; suivant : 006739Hyper-activated IRF-1 and STAT1 contribute to enhanced interferon stimulated gene (ISG) expression by interferon alpha and gamma co-treatment in human hepatoma cells.
Auteurs : Xiao-Nan Zhang [République populaire de Chine] ; Jiang-Xia Liu ; Yun-Wen Hu ; Hui Chen ; Zheng-Hong YuanSource :
- Biochimica et biophysica acta [ 0006-3002 ]
Descripteurs français
- KwdFr :
- Carcinome hépatocellulaire (génétique), Carcinome hépatocellulaire (métabolisme), Dimérisation, Expression des gènes (), Facteur de transcription STAT-1 (), Facteur de transcription STAT-1 (métabolisme), Facteur-1 de régulation d'interféron (antagonistes et inhibiteurs), Facteur-1 de régulation d'interféron (génétique), Facteur-1 de régulation d'interféron (métabolisme), Humains, Interféron de type I (pharmacologie), Interféron gamma (pharmacologie), Lignée cellulaire tumorale, Petit ARN interférent (génétique), Phosphorylation, Protéines proto-oncogènes c-bcl-2 (génétique), Protéines recombinantes, Régions promotrices (génétique), Séquence nucléotidique, Transfection, Tumeurs du foie (génétique), Tumeurs du foie (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Facteur-1 de régulation d'interféron.
- génétique : Carcinome hépatocellulaire, Facteur-1 de régulation d'interféron, Petit ARN interférent, Protéines proto-oncogènes c-bcl-2, Tumeurs du foie.
- métabolisme : Carcinome hépatocellulaire, Facteur de transcription STAT-1, Facteur-1 de régulation d'interféron, Tumeurs du foie.
- pharmacologie : Interféron de type I, Interféron gamma.
- Dimérisation, Expression des gènes, Facteur de transcription STAT-1, Humains, Lignée cellulaire tumorale, Phosphorylation, Protéines recombinantes, Régions promotrices (génétique), Séquence nucléotidique, Transfection.
English descriptors
- KwdEn :
- Base Sequence, Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (metabolism), Cell Line, Tumor, Dimerization, Gene Expression (drug effects), Humans, Interferon Regulatory Factor-1 (antagonists & inhibitors), Interferon Regulatory Factor-1 (genetics), Interferon Regulatory Factor-1 (metabolism), Interferon Type I (pharmacology), Interferon-gamma (pharmacology), Liver Neoplasms (genetics), Liver Neoplasms (metabolism), Phosphorylation, Promoter Regions, Genetic, Proto-Oncogene Proteins c-bcl-2 (genetics), RNA, Small Interfering (genetics), Recombinant Proteins, STAT1 Transcription Factor (chemistry), STAT1 Transcription Factor (metabolism), Transfection.
- MESH :
- chemical , antagonists & inhibitors : Interferon Regulatory Factor-1.
- chemical , chemistry : STAT1 Transcription Factor.
- drug effects : Gene Expression.
- genetics : Carcinoma, Hepatocellular, Interferon Regulatory Factor-1, Liver Neoplasms, Proto-Oncogene Proteins c-bcl-2, RNA, Small Interfering.
- metabolism : Carcinoma, Hepatocellular, Interferon Regulatory Factor-1, Liver Neoplasms, STAT1 Transcription Factor.
- chemical , pharmacology : Interferon Type I, Interferon-gamma.
- Base Sequence, Cell Line, Tumor, Dimerization, Humans, Phosphorylation, Promoter Regions, Genetic, Recombinant Proteins, Transfection.
Abstract
Previous reports suggest that type I and type II Interferon can co-operatively inhibit some virus replication, e.g. HCV, SARS-CoV, HSV-1. To find out the molecular mechanism underlying this phenomenon, we analyzed the transcription profile stimulated by IFN-alpha and IFN-gamma in Huh-7 cells and found that the transcription of a subset of IFN stimulated genes (ISGs) including BclG, XAF1, TRAIL and TAP1 was enhanced when IFN-alpha and gamma were both present. Promoter analysis of BclG revealed that IRF-1 and STAT1 were both required in this process. Enhanced IRF-1/DNA complex formation was observed in interferon co-treatment group by gel shift analysis. Furthermore, IRF-1 activation was found to be generally required in this cluster of ISGs. STAT1 tyrosine phosphorylation was elevated by IFN combination treatment, however, only the hyper-transactivation of GAS but not ISRE was observed. In conclusion, hyper-activation of IRF-1 and elevated STAT1 dimer formation may be two general switches which contribute to a much more robust antiviral symphony against virus replication when type I and type II IFNs are co-administered.
DOI: 10.1016/j.bbaexp.2006.08.003
PubMed: 16987558
Affiliations:
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Le document en format XML
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Microbiology and Biomedical Sciences, Shanghai Medical College, Fudan University, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Medical Molecular Virology, Institute of Microbiology and Biomedical Sciences, Shanghai Medical College, Fudan University</wicri:regionArea><wicri:noRegion>Fudan University</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Jiang Xia" sort="Liu, Jiang Xia" uniqKey="Liu J" first="Jiang-Xia" last="Liu">Jiang-Xia Liu</name></author><author><name sortKey="Hu, Yun Wen" sort="Hu, Yun Wen" uniqKey="Hu Y" first="Yun-Wen" last="Hu">Yun-Wen Hu</name></author><author><name sortKey="Chen, Hui" sort="Chen, Hui" uniqKey="Chen H" first="Hui" last="Chen">Hui Chen</name></author><author><name sortKey="Yuan, Zheng Hong" sort="Yuan, Zheng Hong" uniqKey="Yuan Z" first="Zheng-Hong" last="Yuan">Zheng-Hong Yuan</name></author></analytic><series><title level="j">Biochimica et biophysica 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(chemistry)</term><term>STAT1 Transcription Factor (metabolism)</term><term>Transfection</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Carcinome hépatocellulaire (génétique)</term><term>Carcinome hépatocellulaire (métabolisme)</term><term>Dimérisation</term><term>Expression des gènes ()</term><term>Facteur de transcription STAT-1 ()</term><term>Facteur de transcription STAT-1 (métabolisme)</term><term>Facteur-1 de régulation d'interféron (antagonistes et inhibiteurs)</term><term>Facteur-1 de régulation d'interféron (génétique)</term><term>Facteur-1 de régulation d'interféron (métabolisme)</term><term>Humains</term><term>Interféron de type I (pharmacologie)</term><term>Interféron gamma (pharmacologie)</term><term>Lignée cellulaire tumorale</term><term>Petit ARN interférent (génétique)</term><term>Phosphorylation</term><term>Protéines proto-oncogènes c-bcl-2 (génétique)</term><term>Protéines recombinantes</term><term>Régions promotrices (génétique)</term><term>Séquence 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Sequence</term><term>Cell Line, Tumor</term><term>Dimerization</term><term>Humans</term><term>Phosphorylation</term><term>Promoter Regions, Genetic</term><term>Recombinant Proteins</term><term>Transfection</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Dimérisation</term><term>Expression des gènes</term><term>Facteur de transcription STAT-1</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Phosphorylation</term><term>Protéines recombinantes</term><term>Régions promotrices (génétique)</term><term>Séquence nucléotidique</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous reports suggest that type I and type II Interferon can co-operatively inhibit some virus replication, e.g. HCV, SARS-CoV, HSV-1. To find out the molecular mechanism underlying this phenomenon, we analyzed the transcription profile stimulated by IFN-alpha and IFN-gamma in Huh-7 cells and found that the transcription of a subset of IFN stimulated genes (ISGs) including BclG, XAF1, TRAIL and TAP1 was enhanced when IFN-alpha and gamma were both present. Promoter analysis of BclG revealed that IRF-1 and STAT1 were both required in this process. Enhanced IRF-1/DNA complex formation was observed in interferon co-treatment group by gel shift analysis. Furthermore, IRF-1 activation was found to be generally required in this cluster of ISGs. STAT1 tyrosine phosphorylation was elevated by IFN combination treatment, however, only the hyper-transactivation of GAS but not ISRE was observed. In conclusion, hyper-activation of IRF-1 and elevated STAT1 dimer formation may be two general switches which contribute to a much more robust antiviral symphony against virus replication when type I and type II IFNs are co-administered.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Chen, Hui" sort="Chen, Hui" uniqKey="Chen H" first="Hui" last="Chen">Hui Chen</name><name sortKey="Hu, Yun Wen" sort="Hu, Yun Wen" uniqKey="Hu Y" first="Yun-Wen" last="Hu">Yun-Wen Hu</name><name sortKey="Liu, Jiang Xia" sort="Liu, Jiang Xia" uniqKey="Liu J" first="Jiang-Xia" last="Liu">Jiang-Xia Liu</name><name sortKey="Yuan, Zheng Hong" sort="Yuan, Zheng Hong" uniqKey="Yuan Z" first="Zheng-Hong" last="Yuan">Zheng-Hong Yuan</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Xiao Nan" sort="Zhang, Xiao Nan" uniqKey="Zhang X" first="Xiao-Nan" last="Zhang">Xiao-Nan Zhang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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