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- W2013598984 abstract "Interferons (IFNs) direct innate and acquired immune responses and, accordingly, are used therapeutically to treat a number of diseases, yet the diverse effects they elicit are not fully understood. Here, we identified the promyelocytic leukemia zinc finger (PLZF) protein as a previously unrecognized component of the IFN response. IFN stimulated an association of PLZF with promyelocytic leukemia protein (PML) and histone deacetylase 1 (HDAC1) to induce a decisive subset of IFN-stimulated genes (ISGs). Consequently, PLZF-deficient mice had a specific ISG expression defect and as a result were more susceptible to viral infection. This susceptibility correlated with a marked decrease in the expression of the key antiviral mediators and an impaired IFN-mediated induction of natural killer cell function. These results provide new insights into the regulatory mechanisms of IFN signaling and the induction of innate antiviral immunity." @default.
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- W2013598984 date "2009-06-01" @default.
- W2013598984 modified "2023-10-16" @default.
- W2013598984 title "Promyelocytic Leukemia Zinc Finger Protein Regulates Interferon-Mediated Innate Immunity" @default.
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- W2013598984 doi "https://doi.org/10.1016/j.immuni.2009.04.013" @default.
- W2013598984 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2711215" @default.
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