CCAAT/enhancer-binding protein-beta regulates interferon-induced transcription through a novel element

¹Marlene and Stewart Greenebaum Cancer Center, Department of Microbiology and Immunology, Molecular and Cellular Biology Program, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

|April 25, 2000

Abstract:

We have described previously a novel interferon (IFN)-responsive cis-acting enhancer element called gamma-IFN-activated transcriptional element (GATE). GATE is distinct from the known IFN-stimulated elements and binds to novel transacting factors. To identify the gamma-IFN-responsive transacting factors that interact with GATE, we have screened a cDNA expression library derived from IFN-gamma-stimulated murine macrophage cell line and isolated three different cDNAs. Among these is a gene coding for the pleiotropic transcription factor, CCAAT/enhancer-binding protein-beta (C/EBP-beta). We report here that the gene for C/EBP-beta binds to GATE and induces gene expression. A mutant C/EBP-beta interferes with the IFN-gamma-stimulated transcription of the ISGF3gamma (p48) promoter. Other members of the C/EBP family do not cause these effects. Interestingly, the expression of C/EBP-beta, not the other members of its family, is induced by IFN-gamma. These studies thus identify a novel role for C/EBP-beta in the IFN-signaling pathways.

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Abstract:

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