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pubmed-article:10027649pubmed:abstractTextInterferons (IFNs) stimulate gene expression to mediate their biological actions. A multimeric transcription factor consisting of STAT1, STAT2 and p48, a DNA binding protein, regulates IFN-alpha/beta stimulated gene expression. Since the cellular level of p48 is also increased by pre-treatment of cells with IFN-gamma, it is also known as ISGF3gamma. To understand how IFN-gamma regulates the expression of the p48 gene, we have previously isolated and characterized the promoter of murine p48 gene and identified a novel gamma-IFN activated transcriptional element (GATE). In this study using several mutant constructs of p48 promoter we have determined that the same element responds to IFN-alpha/beta treatment. Relatively high doses of IFN-alpha/beta compared to IFN-gamma are required for the induction of p48 promoter. This ability of IFN-alpha/beta to regulate GATE dependent gene expression is linked to the activation of a factor induced by IFN-alpha. However, IFN-gamma induces the binding of two gamma-IFN inducible factors (GIFs) to GATE. The IFN-alpha inducible GATE binding factor is not recognized by specific antibodies raised against the known IFN-regulated factors. It is likely IFN-gamma is a stronger inducer of this gene because it activates two GIFs. GATE-like elements present in hither to undefined IFN-stimulated genes may control IFN-responses in a unique manner.lld:pubmed
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pubmed-article:10027649pubmed:pagination145-53lld:pubmed
pubmed-article:10027649pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:10027649pubmed:year1999lld:pubmed
pubmed-article:10027649pubmed:articleTitleRegulation of interferon-alpha/beta-stimulated gene expression through the gamma-activated transcriptional element.lld:pubmed
pubmed-article:10027649pubmed:affiliationGreenebaum Cancer Center, Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore 21201, USA.lld:pubmed
pubmed-article:10027649pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10027649pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed