p120-catenin promotes innate antiviral immunity through stabilizing TBK1-IRF3 complex
Copyright © 2023. Published by Elsevier Ltd..
TBK1-IRF3 complex plays vital roles in antiviral immune responses, its regulatory mechanisms are currently incompletely understood. p120-catenin (p120), an armadillo-repeat protein, mainly regulates the stability of classical cadherins and the development of epithelial-to-mesenchymal transitions (EMTs). Here we report that p120 is a positive regulator of type I IFN production. Ectopic expression of p120 enhanced Vesicular stomatitis virus and Sendai-virus-induced type I IFN production, whereas knockdown of p120 expression suppressed type I IFN production. Mechanistically, p120 promoted phosphorylation of IRF3 via stabilizing the TBK1-IRF3 complex. Consistently, p120 knock down mice are more susceptible to VSV infection as indicated by higher tissue viral titers, less IFN-I production and greater infiltration of immune cells. This study reveals p120 as an important positive regulator in innate immunity and identifies that p120 facilitates host antiviral response through stabilizing TBK1-IRF3 complex.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2023 |
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Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:157 |
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Enthalten in: |
Molecular immunology - 157(2023) vom: 15. Mai, Seite 8-17 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Wu, Haifeng [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 01.05.2023 Date Revised 09.05.2023 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.molimm.2023.03.013 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM354633015 |
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520 | |a TBK1-IRF3 complex plays vital roles in antiviral immune responses, its regulatory mechanisms are currently incompletely understood. p120-catenin (p120), an armadillo-repeat protein, mainly regulates the stability of classical cadherins and the development of epithelial-to-mesenchymal transitions (EMTs). Here we report that p120 is a positive regulator of type I IFN production. Ectopic expression of p120 enhanced Vesicular stomatitis virus and Sendai-virus-induced type I IFN production, whereas knockdown of p120 expression suppressed type I IFN production. Mechanistically, p120 promoted phosphorylation of IRF3 via stabilizing the TBK1-IRF3 complex. Consistently, p120 knock down mice are more susceptible to VSV infection as indicated by higher tissue viral titers, less IFN-I production and greater infiltration of immune cells. This study reveals p120 as an important positive regulator in innate immunity and identifies that p120 facilitates host antiviral response through stabilizing TBK1-IRF3 complex | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Zhao, Liang |e verfasserin |4 aut | |
700 | 1 | |a Li, Xiang |e verfasserin |4 aut | |
700 | 1 | |a Li, Ximing |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Yi |e verfasserin |4 aut | |
700 | 1 | |a Gu, Changping |e verfasserin |4 aut | |
700 | 1 | |a Yang, Fan |e verfasserin |4 aut | |
700 | 1 | |a Yan, Jingting |e verfasserin |4 aut | |
700 | 1 | |a Lou, Yalin |e verfasserin |4 aut | |
700 | 1 | |a Li, Yufei |e verfasserin |4 aut | |
700 | 1 | |a Yang, Li |e verfasserin |4 aut | |
700 | 1 | |a Qin, Xiaofeng |e verfasserin |4 aut | |
700 | 1 | |a Wang, Yuelan |e verfasserin |4 aut | |
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