Virus infection of numerous cell types results in the transcriptional induction of a subset of virus- and interferon (IFN)-stimulated genes. The beta IFN (IFN-β) gene is one of these rapidly induced genes; it serves as a fundamental component of the cellular defense response in eliciting potent antiviral, immunomodulatory, and antiproliferative effects. One of the transcription factors involved in the stringent regulation of IFN-β production following virus infection is interferon regulatory factor (IRF) 3 (IRF-3). We have characterized an alternatively spliced isoform of IRF-3 that we have called IRF-3a. IRF-3a can selectively and potently inhibit virus-induced activation of the IFN-β promoter. IRF-3a lacks half of the DNA binding domain found in IRF-3 and is unable to bind to the classical IRF binding elements, IFN-stimulated response elements. These studies suggest that IRF-3a may act as a modulator of IRF-3.
CITATION STYLE
Karpova, A. Y., Ronco, L. V., & Howley, P. M. (2001). Functional Characterization of Interferon Regulatory Factor 3a (IRF-3a), an Alternative Splice Isoform of IRF-3. Molecular and Cellular Biology, 21(13), 4169–4176. https://doi.org/10.1128/mcb.21.13.4169-4176.2001
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