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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

IFN-gamma-stimulated transcriptional activation by IFN-gamma-activated transcriptional element-binding factor 1 occurs via an inducible interaction with CAAAT/enhancer-binding protein-beta.

IFN-gamma- activated transcriptional element (GATE)- binding factor 1 ( GBF1) was identified as a transactivator that induces gene expression through GATE, a novel IFN-inducible element. Although it can induce gene expression, it is an extremely weak DNA-binding protein on its own. GATE also binds another transcription factor, C/ EBP-beta. Therefore, we explored whether GBF1 physically interacts with C/ EBP-beta to induce IFN-gamma-regulated transcription. In response to IFN-gamma, C/ EBP-beta undergoes phosphorylation at a critical ERK1/2 phosphorylation motif. Mutational inactivation of this motif and/or interference with the ERK1/2 activation prevented the IFN-gamma- induced interactions between GBF1 and C/ EBP-beta. A 37-aa long peptide derived from the GBF1 protein can associate with C/ EBP-beta in an IFN-inducible manner. These results identify a converging point for two transactivators that exert their effects through a single response element. Together, our studies identify a novel regulatory mechanism that controls IFN-induced transcription.[1]

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