ILF3 contributes to the establishment of the antiviral type I interferon program.
A549 Cells
Apoptosis Regulatory Proteins
/ genetics
Chemokine CCL5
/ genetics
Chemokine CXCL10
/ genetics
Cytokines
/ genetics
DEAD Box Protein 58
/ genetics
Gene Expression Regulation
HeLa Cells
Host-Pathogen Interactions
/ genetics
Humans
Interferon-beta
/ genetics
Intracellular Signaling Peptides and Proteins
/ genetics
Nuclear Factor 90 Proteins
/ genetics
Poly I-C
/ pharmacology
Polyribosomes
/ drug effects
Protein Biosynthesis
RNA, Double-Stranded
/ antagonists & inhibitors
RNA, Messenger
/ genetics
RNA, Viral
/ antagonists & inhibitors
RNA-Binding Proteins
/ genetics
Receptors, Immunologic
Signal Transduction
Ubiquitins
/ genetics
Virus Replication
Journal
Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011
Informations de publication
Date de publication:
10 01 2020
10 01 2020
Historique:
accepted:
04
11
2019
revised:
21
10
2019
received:
16
05
2019
pubmed:
9
11
2019
medline:
19
3
2020
entrez:
9
11
2019
Statut:
ppublish
Résumé
Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1, and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised.
Identifiants
pubmed: 31701124
pii: 5614571
doi: 10.1093/nar/gkz1060
pmc: PMC7145544
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
CCL5 protein, human
0
CXCL10 protein, human
0
Chemokine CCL5
0
Chemokine CXCL10
0
Cytokines
0
IFIT2 protein, human
0
IFIT3 protein, human
0
ILF3 protein, human
0
Intracellular Signaling Peptides and Proteins
0
Nuclear Factor 90 Proteins
0
RNA, Double-Stranded
0
RNA, Messenger
0
RNA, Viral
0
RNA-Binding Proteins
0
Receptors, Immunologic
0
Ubiquitins
0
ISG15 protein, human
60267-61-0
Interferon-beta
77238-31-4
RIGI protein, human
EC 3.6.1.-
DEAD Box Protein 58
EC 3.6.4.13
Poly I-C
O84C90HH2L
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
116-129Subventions
Organisme : Wellcome Trust
ID : 107665/Z/15/Z
Pays : United Kingdom
Informations de copyright
© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.
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