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.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Ma Z,Moore R,Xu X,Barber GNdoi
10.1371/journal.ppat.1003721subject
Has Abstractpub_date
2013-10-01 00:00:00pages
e1003721issue
10eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-13-00847journal_volume
9pub_type
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