Correction: DDX56 inhibits type I interferon by disrupting assembly of IRF3-IPO5 to inhibit IRF3 nucleus import
Autor: | Li, Dan, Fu, Shaozu, Wu, Zhengqian, Yang, Wenping, Ru, Yi, Shu, Hongbing, Liu, Xiangtao, Zheng, Haixue |
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Rok vydání: | 2020 |
Předmět: |
IPO5
THP-1 Cells viruses Active Transport Cell Nucleus Protein Serine-Threonine Kinases Respirovirus Infections Sendai virus DEAD-box RNA Helicases Gene Knockout Techniques Humans Phosphorylation DDX56 Type I interferon Cell Nucleus Correction virus diseases Interferon-beta Cell Biology biochemical phenomena metabolism and nutrition IRF3 beta Karyopherins Immunity Innate HEK293 Cells Interferon Regulatory Factor-3 Nucleus import HeLa Cells Signal Transduction Research Article |
Zdroj: | Journal of Cell Science article-version (VoR) Version of Record |
ISSN: | 1477-9137 |
Popis: | Transcription factor IRF3-mediated type I interferon induction plays a role in antiviral innate immunity. However, mechanisms for the control and regulation of IRF3 nuclear import remain largely unknown. We have identified DEAD box polypeptide 56 (DDX56) as a negative regulator of virus-triggered IFN-β induction. Overexpression of DDX56 suppressed nuclear translocation of IRF3 via disrupting the IRF3–IOP5 interaction, whereas knockdown or knockout of DDX56 had the opposite effect. In addition, the interaction between DDX56 and IRF3 increased during viral infection. We further found that the D166 site of DDX56 was essential for inhibiting IRF3 import into the nucleus. Our findings suggest that DDX56 regulates antiviral innate immunity by inhibiting the nuclear translocation of IRF3, revealing a novel mechanism of the DDX56-mediated innate antiviral response. This article has an associated First Person interview with the first author of the paper. Summary: DDX56 is a negative regulator of virus-triggered IFN-β induction that acts by disruputing the IRF3–IOP5 interaction to inhibit the import of IRF3 into the nucleus. |
Databáze: | OpenAIRE |
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