Journal
EMBO JOURNAL
Volume 27, Issue 15, Pages 2135-2146Publisher
WILEY
DOI: 10.1038/emboj.2008.126
Keywords
DDX3X; innate immunity; interferon; phosphorylation; TBK1
Categories
Funding
- Austrian Science Fund (FWF) [F 2803] Funding Source: researchfish
- Austrian Science Fund FWF [F 2803, P 17859, P 20522] Funding Source: Medline
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TANK-binding kinase 1 (TBK1) is of central importance for the induction of type-I interferon (IFN) in response to pathogens. We identified the DEAD-box helicase DDX3X as an interaction partner of TBK1. TBK1 and DDX3X acted synergistically in their ability to stimulate the IFN promoter, whereas RNAi-mediated reduction of DDX3X expression led to an impairment of IFN production. Chromatin immunoprecipitation indicated that DDX3X is recruited to the IFN promoter upon infection with Listeria monocytogenes, suggesting a transcriptional mechanism of action. DDX3X was found to be a TBK1 substrate in vitro and in vivo. Phosphorylation-deficient mutants of DDX3X failed to synergize with TBK1 in their ability to stimulate the IFN promoter. Overall, our data imply that DDX3X is a critical effector of TBK1 that is necessary for type I IFN induction.
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