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- W1982177785 abstract "Herpes simplex virus 1 (HSV-1) is able to induce interferon-α production by natural IFN-α-producing cells. In this study, signal transduction in this process was examined. It was found that sequestering of calcium by EGTA abolished IFN-α induction by HSV-infected cells. Stimulation of human PBMC by HSV-1-infected fibroblasts resulted in the production of inositol triphosphate (InsP3) and tyrosine phosphorylation of cellular proteins. The protein kinase C inhibitor, H7, and the tyrosine kinase inhibitor, herbimycin A, were able to suppress IFN-α gene expression as determined by IFN bioassay and RT-PCR. An IFN-α-specific ELISpot assay revealed that herbimycin A and H7 remarkably decreased the number of IFN-α-producing cells. PMA or calcium ionophore A23187 alone did not increase IFN-α production. However, PMA in conjugation with ionophores increased IFN-α production as early as 2 h. HA1004 and 2′,5′-dideoxyadenosine, which are potent inhibitors of PKA pathway, had no effect on IFN-α production. In contrast, BrcAMP, a specific PKA activator, inhibited the IFN-α secretion and number of IFN-α-producing cells and to a lesser extent reduced the level of IFN-α mRNA. Our results indicate that protein kinase C, tyrosine kinases, and protein kinase A are involved in the regulation of IFN-α production in response to HSV-1." @default.
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- W1982177785 date "1996-02-01" @default.
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- W1982177785 title "Role of Tyrosine Kinases, Protein Kinase C, and Protein Kinase A in the Regulation of Interferon-α Production Induced by Herpes Simplex Virus Type 1" @default.
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- W1982177785 doi "https://doi.org/10.1089/jir.1996.16.109" @default.
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