The alpha beta interferons (IFNs) transiently induce genes through an IFN-stimulable DNA response element (ISRE). IFN-cell surface receptor interaction triggers the cytoplasmic activation of the complex primary transcription factor E, which on translocation and interaction with the ISRE initiates transcription. Whether E is activated directly through the receptor(s) or through a more classical second message pathway(s) and the roles of additional factors in the alpha beta and gamma IFN responses remain to be established. Meanwhile analysis of mutants has revealed complexity and overlap in the alpha, beta and gamma IFN response pathways and the products of at least two viruses have been shown to inhibit IFN-inducible gene expression.
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