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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Expression of gamma interferon-dependent genes is blocked independently by virion host shutoff RNase and by US3 protein kinase.

Gamma interferon receptor alpha (IFN-gammaR alpha) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-gammaR alpha is phosphorylated by the U(S)3 kinase. The modification is abolished in cells infected with DeltaU(S)3, DeltaU(L)13, or Delta(U(S)3/U(L)13) mutant virus. Transcripts of the IFN-gamma-dependent genes do not accumulate in cells transduced with the U(S)3 protein kinase and treated with IFN-gamma. In contrast, the accumulation of IFN-gamma-dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the DeltaU(S)3 mutant virus, and to a lesser extent in the DeltaU(L)41 virus-infected cells. The accumulation of IFN-gamma-dependent gene transcripts in DeltaU(L)41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U(S)3 protein. The results suggest that the expression of IFN-gamma-dependent genes is blocked independently by the degradation of IFN-gamma-dependent gene transcripts--a function of the virion host shutoff RNase--and by posttranslational modification of the IFN-gammaR alpha protein.[1]


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