Molecular and Cellular Biology, July 2001, p. 4169-4176, Vol. 21, No. 13
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.13.4169-4176.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
andDepartment of Pathology, Harvard Medical School, Boston, Massachusetts 021151
Received 30 November 2000/Returned for modification 22 January 2001/Accepted 30 March 2001
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-
) 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-
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-
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.
Present address: Pfizer Inc., Discovery Technology Center,
Cambridge, MA 02139.
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