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Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells

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-α and IFN-γ in Huh-7 cells and found that...

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Autores principales: Zhang, Xiao-Nan, Liu, Jiang-Xia, Hu, Yun-Wen, Chen, Hui, Yuan, Zheng-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7148893/
https://www.ncbi.nlm.nih.gov/pubmed/16987558
http://dx.doi.org/10.1016/j.bbaexp.2006.08.003
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author Zhang, Xiao-Nan
Liu, Jiang-Xia
Hu, Yun-Wen
Chen, Hui
Yuan, Zheng-Hong
author_facet Zhang, Xiao-Nan
Liu, Jiang-Xia
Hu, Yun-Wen
Chen, Hui
Yuan, Zheng-Hong
author_sort Zhang, Xiao-Nan
collection PubMed
description 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-α and IFN-γ 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-α and γ 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.
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spelling pubmed-71488932020-04-13 Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells Zhang, Xiao-Nan Liu, Jiang-Xia Hu, Yun-Wen Chen, Hui Yuan, Zheng-Hong Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression Article 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-α and IFN-γ 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-α and γ 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. Elsevier B.V. 2006 2006-08-12 /pmc/articles/PMC7148893/ /pubmed/16987558 http://dx.doi.org/10.1016/j.bbaexp.2006.08.003 Text en Copyright © 2006 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Zhang, Xiao-Nan
Liu, Jiang-Xia
Hu, Yun-Wen
Chen, Hui
Yuan, Zheng-Hong
Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title_full Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title_fullStr Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title_full_unstemmed Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title_short Hyper-activated IRF-1 and STAT1 contribute to enhanced Interferon stimulated gene (ISG) expression by Interferon α and γ co-treatment in human hepatoma cells
title_sort hyper-activated irf-1 and stat1 contribute to enhanced interferon stimulated gene (isg) expression by interferon α and γ co-treatment in human hepatoma cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7148893/
https://www.ncbi.nlm.nih.gov/pubmed/16987558
http://dx.doi.org/10.1016/j.bbaexp.2006.08.003
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