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IFN--Stimulated Transcriptional Activation by IFN--Activated Transcriptional Element-Binding Factor 1 Occurs via an Inducible Interaction with CAAAT/Enhancer-Binding Protein-¹

Qingjun Meng^*, Abhijit Raha^*, Sanjit Roy^*, Junbo Hu and Dhananjaya V. Kalvakolanu^2,*

^* Greenebaum Cancer Center, Department of Microbiology and Immunology, Molecular and Cellular Biology Graduate Program, University of Maryland School of Medicine, Baltimore, MD 21201; and Department of Surgery, Tongji Medical Center, Huazhong University of Science and Technology, Wuhan, People’s Republic of China

IFN--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-. Therefore, we explored whether GBF1 physically interacts with C/EBP- to induce IFN--regulated transcription. In response to IFN-, C/EBP- 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--induced interactions between GBF1 and C/EBP-. A 37-aa long peptide derived from the GBF1 protein can associate with C/EBP- 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.

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The JI 2005 174: 5905-5906. [Full Text]  

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