The DEAD-box helicase DDX3X is a critical component of the TANK-binding kinase 1-dependent innate immune response

Didier Soulat ^[1] ; Tilmann Bürckstümmer ^[2] ; Sandra Westermayer ^[1] ; Adriana Goncalves ^[2] ; Angela Bauch ^[2] ; Adrijana Stefanovic ^[2] ; Oliver Hantschel ^[2] ; Keiryn L Bennett ^[2] ; Thomas Decker ^[1] ; Giulio Superti-Furga ^[2]
1. [1] University of Vienna
  
  University of Vienna
  
  Innere Stadt, Austria
2. [2] Austrian Academy of Sciences
  
  Austrian Academy of Sciences
  
  Innere Stadt, Austria
Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 27, Nº. 15, 2008, págs. 2135-2146
Idioma: inglés
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Resumen
- 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.