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pubmed-article:11070172pubmed:abstractTextInduction of the interferon (IFN)-alpha/beta gene transcription in virus-infected cells is an event central to innate immunity. Mice lacking the transcription factor IRF-3 are more vulnerable to virus infection. In embryonic fibroblasts, virus-induced IFN-alpha/beta gene expression levels are reduced and the spectrum of the IFN-alpha mRNA subspecies altered. Furthermore, cells additionally defective in IRF-7 expression totally fail to induce these genes in response to infections by any of the virus types tested. In these cells, a normal profile of IFN-alpha/beta mRNA induction can be achieved by coexpressing both IRF-3 and IRF-7. These results demonstrate the essential and distinct roles of thetwo factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.lld:pubmed
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pubmed-article:11070172pubmed:articleTitleDistinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction.lld:pubmed
pubmed-article:11070172pubmed:affiliationDepartment of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Japan.lld:pubmed
pubmed-article:11070172pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11070172pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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