DDX24 Negatively Regulates Cytosolic RNA-Mediated Innate Immune Signaling

Zhe Ma, Robert Moore, Xiangxi Xu, Glen N Barber

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

RIG-I-Like Receptors (RLRs) sense cytosolic viral RNA to transiently activate type I IFN production. Here, we report that a type I IFN inducible DExD/H helicase, DDX24, exerts a negative-regulatory effect on RLR function. Expression of DDX24 specifically suppressed RLR activity, while DDX24 loss, which caused embryonic lethality, augmented cytosolic RNA-mediated innate signaling and facilitated RNA virus replication. DDX24 preferentially bound to RNA rather than DNA species and influenced signaling by associating with adaptor proteins FADD and RIP1. These events preferentially impeded IRF7 activity, an essential transcription factor for type I IFN production. Our data provide a new function for DDX24 and help explain innate immune gene regulation, mechanisms that may additionally provide insight into the causes of inflammatory disease.

Original languageEnglish
Article numbere1003721
JournalPLoS Pathogens
Volume9
Issue number10
DOIs
StatePublished - Oct 1 2013

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RNA
RNA Viruses
Viral RNA
Virus Replication
Transcription Factors
DNA
Genes
Proteins

ASJC Scopus subject areas

  • Microbiology
  • Parasitology
  • Virology
  • Immunology
  • Genetics
  • Molecular Biology

Cite this

DDX24 Negatively Regulates Cytosolic RNA-Mediated Innate Immune Signaling. / Ma, Zhe; Moore, Robert; Xu, Xiangxi; Barber, Glen N.

In: PLoS Pathogens, Vol. 9, No. 10, e1003721, 01.10.2013.

Research output: Contribution to journalArticle

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