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J Biol Chem, Vol. 273, Issue 44, 29210-29217, October 30, 1998
From the The family of interferon regulatory factors
(IRFs) plays an important role in modulating cellular responses to
viral infection and cytokines, including IFNs. The transcription
factors that are involved in the transcriptional activation of the IFNB
gene have been extensively studied. However, the molecular mechanism by
which virus activates the expression of the IFNA gene remains to be
defined. Recently, we have identified a new IRF-7 isoform, denoted as
IRF-7H, which encodes a protein of 514 amino acids and is most closely
related to the IRF-3. The expression of IRF-7 is restricted to the
lymphoid cell types and is inducible by virus, lipopolysaccharide,
and IFNA. The functional characterization of IRF-7H reveals a presence
of transactivation domain located carboxyl-terminal to its DNA binding
domain. Overexpression of IRF-7H results in an activation of IFNA
promoter in transient transfection assay and a strong enhancement of
virus-mediated activation of this promoter. Whereas in uninfected
cells, overexpressed IRF-7H is present mainly in the cytoplasm, viral
infection facilitates the transfer of IRF-7H to the nucleus;
overexpression of IRF-3 interferes with the virus-induced translocation
of IRF-7H. Thus, IRF-7 exhibits functional similarity to IRF-3;
however, the preferential expression of IRF-7 in lymphoid cells (the
cell type that expresses IFNA) suggests that IRF-7 may play a critical
role in regulating the IFNA gene expression.
Characterization of the Interferon Regulatory Factor-7 and
Its Potential Role in the Transcription Activation of Interferon A
Genes
,, and¶
Oncology Center and the ¶ Department of
Molecular Biology and Genetics, The Johns Hopkins University School of
Medicine, Baltimore, Maryland 21231 and § Human Genome
Sciences, Inc., Rockville, Maryland 20850
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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