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J. Biol. Chem., Vol. 268, Issue 32, 24032-24040, 11, 1993
WC Au, Y Su, NB Raj and PM Pitha
Transcriptional activation of interferon A (IFNA) gene in virus- infected
cells is controlled by a 35-nucleotide inducible element that is cell type
specific. Within this region, two elements, alpha F1 and IRF-1 binding
sites, were shown by mutation analysis to play a crucial role in the
expression of inducible element. In this study, we have analyzed the
binding of nuclear proteins to the alpha F1 sequence and have shown that
the induction is associated with the formation of a novel complex alpha
F1/B, which contains at least two DNA binding proteins of 68 and 96 kDa. In
contrast, no binding of the purified interferon regulatory factor 1 (IRF-1)
either to the alpha F1 or IRF-1 binding sites could be detected in vitro.
However, the oligonucleotides corresponding to alpha F1 or IRF-1 binding
sites competed efficiently for the induction of IFNA4 promoter region in a
transient transfection assay. We suggest that the induction of IFNA
promoter region requires cooperation between alpha F1 binding proteins and
IRF-1. Interestingly, our data also show that the inability of IFNA6
promoter to be expressed in infected L-cells may be a result of a
viral-induced repressor, which could act by binding and inactivating alpha
F1 or by competing for the IRF-1 binding site. These results suggest that
cell-specific expression of IFNA genes results from core-cruitment of
trans-acting factors that bind to alpha F1 and the IRF-1 binding site with
the cell-specific virus-induced activator or repressor.
Virus-mediated induction of interferon A gene requires cooperation between multiple binding factors in the interferon alpha promoter region
Oncology Center, Johns Hopkins University, Baltimore, Maryland 21231.
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