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Regulation of NO Synthesis, Local Inflammation, and Innate Immunity to Pathogens by BET Loved ones ProteinsSebastian Wienerroither,a Isabella Rauch,a Felix Rosebrock,a Amanda M. Jamieson,a James Bradner,b Matthias Muhar,c Johannes Zuber,c Mathias M ler,d Thomas DeckeraMax F. Perutz Laboratories, University of Vienna, Vienna, Austriaa; Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Healthcare School, Boston, Massachusetts, USAb; Institute of Molecular Pathology, Vienna, Austriac; Institute of Animal Breeding, University of Veterinary Medicine Vienna, Vienna, AustriadTranscriptional activation in the Nos2 gene, encoding inducible GLUT4 custom synthesis nitric oxide synthase (iNOS), through infection or irritation needs coordinate assembly of an initiation complicated through the transcription elements NF- B and form I interferon-activated ISGF3. Here we present that infection of macrophages with the intracellular bacterial pathogen Listeria monocytogenes triggered binding of the BET proteins Brd2, Brd3, and, most prominently, Brd4 towards the Nos2 promoter and that a profound reduction of Nos2 expression occurred within the presence on the BET inhibitor JQ1. RNA polymerase activity on the Nos2 gene was regulated by means of Brdmediated C-terminal domain (CTD) phosphorylation at serine five. Underscoring the essential value of Brd for that regulation of immune responses, application of JQ1 reduced NO production in mice contaminated with L. monocytogenes, too as innate resistance to L. monocytogenes and influenza virus. In the murine model of inflammatory illness, JQ1 treatment enhanced the colitogenic.