MG132 Attenuates the Replication of Classical Swine Fever Virus
26S proteasome
JAK-STAT pathway
MG132
STAT1
classical swine fever virus
Journal
Frontiers in microbiology
ISSN: 1664-302X
Titre abrégé: Front Microbiol
Pays: Switzerland
ID NLM: 101548977
Informations de publication
Date de publication:
2020
2020
Historique:
received:
29
11
2019
accepted:
09
04
2020
entrez:
26
6
2020
pubmed:
26
6
2020
medline:
26
6
2020
Statut:
epublish
Résumé
The 26S proteasome, in charge of intracellular protein degradation, plays significant roles in the modulation of various cellular activities as well as in the interplay between virus and host. However, studies about the relationship between 26S proteasome and classical swine fever virus (CSFV) is limited up to now. MG132 is a proteasome inhibitor and has been extensively used in studies about replication of many viruses. Herein, we investigated the role of MG132 in CSFV replication and results showed that MG132 significantly decreased virus titers and viral RNA copies in CSFV-infected PK-15 cells. Further studies demonstrated that MG132 upregulated the expression of several interferon-stimulated genes (ISGs), in CSFV-infected cells. Since the activation of ISGs is controlled by the JAK-STAT signal pathway, we next examined the effect of MG132 on the expression and localization of key molecular STAT1 in the infected cells using Western blot and confocal laser scanning microscopy, respectively. Results showed that CSFV infection and viral NS4A protein decreased the protein level of STAT1, and MG132 promoted the accumulation of STAT1 in the nucleus of cells adjacent to the CSFV-infected cells. Besides, MG132 did not affect the expressions of
Identifiants
pubmed: 32582037
doi: 10.3389/fmicb.2020.00852
pmc: PMC7283581
doi:
Types de publication
Journal Article
Langues
eng
Pagination
852Informations de copyright
Copyright © 2020 Chen, Fan, Zhao, Wu, Zhu, Ma, He, Deng, Xu, Zhang, Ding, Yi, Zhao and Chen.
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