ATG13 restricts viral replication by induction of type I interferon

Intriguingly, ATG5‐ATG12 positively regulated antiviral NF‐κB and IRF3 signalling during foot‐and‐mouth disease virus infection. [...]Mauthe et al conduct an unbiased RNA interference screen approach to explore unconventional functions of ATG proteins during viral infections. In order to identify po...

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Published inJournal of cellular and molecular medicine Vol. 23; no. 9; pp. 6508 - 6511
Main Authors Du, Jiang‐long, Ma, Peng, Wang, Chen, Zeng, Yan, Xue, Yu‐jia, Yang, Xue‐cai, Wan, Xue‐mei, Chang, Fan‐fan, Zhao, Tian‐yu, Jia, Xiao‐ye, Wang, Hai‐zhen, Liu, Jing, Ma, Zhong‐ren, Cao, Xin, Cai, Kui‐zheng
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.09.2019
John Wiley and Sons Inc
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Summary:Intriguingly, ATG5‐ATG12 positively regulated antiviral NF‐κB and IRF3 signalling during foot‐and‐mouth disease virus infection. [...]Mauthe et al conduct an unbiased RNA interference screen approach to explore unconventional functions of ATG proteins during viral infections. In order to identify possible roles for ATG13 in antiviral immunity, we transfected human embryonic kidney cells HEK293T (293T cells) with an IFN‐sensitive response element (ISRE) luciferase reporter, which was an interferon regulatory factor 3 (IRF3)‐dependent promoter, and the internal control renilla luciferase, as well as expression vectors containing ATG13. The overexpression of ATG13 with the retinoic acid‐inducible gene‐I (RIG‐I)‐like receptors (RLRs) signalling proteins, including RIG‐I, melanoma differentiation‐associated antigen 5 (MDA5), mitochondrial antiviral signalling (MAVS), tumor necrosis factor (TNF) receptor associated factor (TRAF) family member associated NF‐κB activator (TANK) binding kinase 1 (TBK1), inhibitor of NF‐κB kinase subunit epsilon (IKKi), IRF3 and stimulator of interferon genes, additively activated ISRE luciferase activity (Figure B). [...]we identified that ATG13 could interact with TRAF3 and TRAF6 by co‐immunoprecipitation assay (Figure L).
Bibliography:Du and Ma contributed equally to this work
SourceType-Scholarly Journals-1
ObjectType-Correspondence-2
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ISSN:1582-1838
1582-4934
1582-4934
DOI:10.1111/jcmm.14483