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- W2980453962 abstract "Abstract Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1 , and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised." @default.
- W2980453962 created "2019-10-25" @default.
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- W2980453962 date "2019-10-17" @default.
- W2980453962 modified "2023-10-14" @default.
- W2980453962 title "ILF3 contributes to the establishment of the antiviral type I interferon program" @default.
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- W2980453962 doi "https://doi.org/10.1101/809608" @default.
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