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• W2081499148 abstract "Expression of the Type I IFN (i.e., IFN- α s and IFN- β ) genes is efficiently induced by viruses at the transcriptional level. This induction is mediated by at least two types of positive regulatory elements located in the human IFN- β gene promoter: (1) the repeated elements which bind both the transcriptional activator IRF-1 and the repressor IRF-2 (IRF-elements; IRF-Es), and (2) the x B element ( x B-E), which binds NF x B and is located between the IRF-Es and the TATA box. In this study we demonstrate that a promoter containing synthetic IRF-E, which displays high affinity for the IRFs can be efficiently activated by Newcastle disease virus (NDV). In contrast, such activation was either very weak or nil when cells were treated by IFN- β or tumor necrosis factor- α (TNF- α ), despite the fact they both efficiently induce de novo synthesis of the short-lived IRF-1 In L929 cells. In fact, efficient activation of the IRF-E apparently requires an event in addition to de novo IRF-1 induction, which can be elicited by NDV even in the presence of protein synthesis inhibitor, cycloheximide. Moreover, efficient activation of the IRF-E by NOV is specifically inhibited by the protein kinase inhibitor, Staurosporin. Hence our results suggest the importance of IRF-1 synthesis and post-translational modification event(s), possibly phosphorylation for the efficient activation of IRF-Es, which are otherwise under negative regulation by IRF-2." @default.
• W2081499148 created "2016-06-24" @default.
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• W2081499148 date "1991-01-01" @default.
• W2081499148 modified "2023-09-25" @default.
• W2081499148 title "Activation of IFN-<i>β</i>element by IRF-1 requires a post-translational event in addition to IRF-1 synthesis" @default.
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• W2081499148 doi "https://doi.org/10.1093/nar/19.16.4421" @default.
• W2081499148 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/328629" @default.
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