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The DEAD‐box helicase DDX3X is a critical component of the TANK‐binding kinase 1‐dependent innate immune response
Author(s) -
Soulat Didier,
Bürckstümmer Tilmann,
Westermayer Sandra,
Goncalves Adriana,
Bauch Angela,
Stefanovic Adrijana,
Hantschel Oliver,
Bennett Keiryn L,
Decker Thomas,
SupertiFurga Giulio
Publication year - 2008
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2008.126
Subject(s) - biology , tank binding kinase 1 , dead box , rna helicase a , innate immune system , chromatin immunoprecipitation , microbiology and biotechnology , irf3 , helicase , kinase , promoter , protein kinase a , gene , gene expression , biochemistry , genetics , immune system , cyclin dependent kinase 2 , rna
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.