| First Author | Wienerroither S | Year | 2015 |
| Journal | Cell Rep | Volume | 12 |
| Issue | 2 | Pages | 300-12 |
| PubMed ID | 26146080 | Mgi Jnum | J:265996 |
| Mgi Id | MGI:6204398 | Doi | 10.1016/j.celrep.2015.06.021 |
| Citation | Wienerroither S, et al. (2015) Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-kappaB Pathways by Concerted Recruitment of the Mediator Complex. Cell Rep 12(2):300-12 |
| abstractText | 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-kappaB pathways. Using ChIP-seq analysis, we define genes induced in Lm-infected macrophages through synergistic transcriptional activation by NF-kappaB and the IFN-I-activated transcription factor ISGF3. Using the Nos2 and IL6 genes as prime examples of this group, we show that NF-kappaB functions to recruit enzymes that establish histone marks of transcriptionally active genes. In addition, NF-kappaB 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-kappaB and the engagement of the core mediator for Pol II binding by ISGF3. |
