CFLIPL Interrupts IRF3-CBP-DNA Interactions To Inhibit IRF3-Driven Transcription.

ABSTRACT: Type I IFN induction is critical for antiviral and anticancer defenses. Proper downregulation of type I IFN is equally important to avoid deleterious imbalances in the immune response. The cellular FLIP long isoform protein (cFLIPL) controls type I IFN production, but opposing publications show it as either an inhibitor or inducer of type I IFN synthesis. Regardless, the mechanistic basis for cFLIPL regulation is unknown. Because cFLIPL is important in immune cell development and proliferation, and is a target for cancer therapies, it is important to identify how cFLIPL regulates type I IFN production. Data in this study show that cFLIPL inhibits IFN regulatory factor 3 (IRF3), a transcription factor central for IFN-β and IFN-stimulated gene expression. This inhibition occurs during virus

SUBMITTER: Gates LT 

PROVIDER: S-EPMC4955763 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature