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AGO2 Negatively Regulates Type I Interferon Signaling Pathway by Competition
Binding IRF3 with CBP/p300
#MMPMID28589097
Wang S
; Sun X
; Yi C
; Zhang D
; Lin X
; Sun X
; Chen H
; Jin M
Front Cell Infect Microbiol
2017[]; 7
(?): 195
PMID28589097
show ga
Viral infection triggers a series of signaling cascades and host innate immune
responses, including interferon (IFN) production, which depends on coordinated
activity of multiple transcription factors. IFN regulatory factor 3 (IRF3) and
transcriptional coactivator CREB binding protein (CBP) and/or p300 are core
factors that participate in transcriptional complex formation in the nucleus. In
general, cells balance the production of IFNs through suppressive and stimulative
mechanisms, but viral infections can disrupt such equilibrium. This study
determined that H5N1 viral infection reduced the distribution of human argonaute
2 (AGO2) in A549 cell nucleus. AGO2 did not block phosphorylation, nuclear
translocation, and DNA binding ability of IRF3 but inhibited its association with
CBP. Therefore, this newly revealed mechanism shows that cellular response leads
to transfer of AGO2 from cell nucleus and promotes IFN-? expression to increase
host survival during viral infection.
|*Signal Transduction
[MESH]
|A549 Cells
[MESH]
|Animals
[MESH]
|Argonaute Proteins/*metabolism
[MESH]
|CREB-Binding Protein/*metabolism
[MESH]
|Cell Nucleus/metabolism
[MESH]
|Cell Proliferation
[MESH]
|Dogs
[MESH]
|E1A-Associated p300 Protein/*metabolism
[MESH]
|HEK293 Cells
[MESH]
|Host-Pathogen Interactions/immunology
[MESH]
|Humans
[MESH]
|Immunity, Innate
[MESH]
|Influenza A Virus, H5N1 Subtype/immunology
[MESH]
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