دورية أكاديمية

DLG1 promotes the antiviral innate immune response by inhibiting p62-mediated autophagic degradation of IKKε.

التفاصيل البيبلوغرافية
العنوان: DLG1 promotes the antiviral innate immune response by inhibiting p62-mediated autophagic degradation of IKKε.
المؤلفون: Chang H; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Wu H; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Hou P; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Aizaz M; Shandong Provincial Key Laboratory of Animal Resistance Biology, College of Life Sciences, Shandong Normal University, Jinan, China., Yang R; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Xiang A; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Qi W; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., He H; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China., Wang H; Ruminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, Shandong, China.
المصدر: Journal of virology [J Virol] 2023 Dec 21; Vol. 97 (12), pp. e0150123. Date of Electronic Publication: 2023 Nov 20.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Society For Microbiology Country of Publication: United States NLM ID: 0113724 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1098-5514 (Electronic) Linking ISSN: 0022538X NLM ISO Abbreviation: J Virol Subsets: MEDLINE
أسماء مطبوعة: Publication: Washington Dc : American Society For Microbiology
Original Publication: Baltimore, American Society for Microbiology.
مواضيع طبية MeSH: Autophagy* , Discs Large Homolog 1 Protein*/metabolism , I-kappa B Kinase*/metabolism , Immunity, Innate*/immunology , Negative-Sense RNA Viruses*/growth & development , Negative-Sense RNA Viruses*/immunology , Sequestosome-1 Protein*/antagonists & inhibitors , Virus Diseases*/immunology, Humans ; Polyubiquitin/metabolism ; Signal Transduction ; Animals ; Cell Line
مستخلص: Importance: The type-I interferon (IFN-I) signaling pathway is the first line of antiviral innate immunity. It must be precisely regulated against virus-induced damage. The tightly regulated mechanisms of action of host genes in the antiviral innate immune signaling pathway are still worth studying. Here, we report a novel role of DLG1 in positively regulating the IκB kinase epsilon (IKKε)-mediated IFN-I signaling response against negative-stranded RNA virus replication, whereas the RNA virus inhibits the expression of DLG1 for immune escape. Importantly, the E3 ligase March2 interacts with and promotes K27-linked polyubiquitination of IKKε, and p62 is a cargo receptor that recognizes ubiquitinated IKKε for eventual autophagic degradation. Together, the current findings elucidate the role of DLG1 in the antiviral IFN-I signaling pathway and viral infection repression.
Competing Interests: The authors declare no conflict of interest.
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معلومات مُعتمدة: 32072834 MOST | National Natural Science Foundation of China (NSFC); 31972665 MOST | National Natural Science Foundation of China (NSFC); tspd20181207 Taishan Scholar Project of Shandong Province; 2022CXGC020711 Key R&D Program of Shandong Province, China; 202228060 Jinan Innovation Team
فهرسة مساهمة: Keywords: DLG1; IKKε; autophagy; innate immunity; interferon; ubiquitination
المشرفين على المادة: 0 (Discs Large Homolog 1 Protein)
0 (DLG1 protein, human)
EC 2.7.11.10 (I-kappa B Kinase)
EC 2.3.2.27 (MARCHF2 protein, human)
120904-94-1 (Polyubiquitin)
0 (Sequestosome-1 Protein)
0 (SQSTM1 protein, human)
تواريخ الأحداث: Date Created: 20231120 Date Completed: 20240102 Latest Revision: 20240102
رمز التحديث: 20240103
مُعرف محوري في PubMed: PMC10734446
DOI: 10.1128/jvi.01501-23
PMID: 37982618
قاعدة البيانات: MEDLINE
الوصف
تدمد:1098-5514
DOI:10.1128/jvi.01501-23