期刊
CELL REPORTS
卷 12, 期 2, 页码 300-312出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.06.021
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资金
- Austrian Science Fund (FWF) [SFB-28]
The transcriptional response to infection with the bacterium Listeria monocytogenes (Lm) requires cooperative signals of the type I interferon (IFN-I)stimulated JAK-STAT and proinflammatory NF-kappa B pathways. Using ChIP-seq analysis, we define genes induced in Lm-infected macrophages through synergistic transcriptional activation by NF-kappa B and the IFN-I-activated transcription factor ISGF3. Using the Nos2 and IL6 genes as prime examples of this group, we show that NF-kappa B functions to recruit enzymes that establish histone marks of transcriptionally active genes. In addition, NF-kappa B regulates transcriptional elongation by employing the mediator kinase module for the recruitment of the pTEFb complex. ISGF3 has a major role in associating the core mediator with the transcription start as a prerequisite for TFIID and RNA polymerase II (Pol II) binding. Our data suggest that the functional cooperation between two major antimicrobial pathways is based on promoter priming by NF-kappa B and the engagement of the core mediator for Pol II binding by ISGF3.
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