RIPLET, and not TRIM25, is required for endogenous RIG-I-dependent antiviral responses.

التفاصيل البيبلوغرافية
العنوان:	RIPLET, and not TRIM25, is required for endogenous RIG-I-dependent antiviral responses.
المؤلفون:	Hayman TJ; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Hsu AC; Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia., Kolesnik TB; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia., Dagley LF; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Willemsen J; Research Group Dynamics of Early Viral Infection and the Innate Antiviral Response, Division Virus-Associated Carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany., Tate MD; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.; Department of Molecular Translational Science, School of Clinical Sciences, Monash University, Clayton, VIC, Australia., Baker PJ; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Kershaw NJ; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Kedzierski L; Department of Microbiology and Immunology, University of Melbourne, Peter Doherty Institute for Infection and Immunity, Parkville, VIC, Australia., Webb AI; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Wark PA; Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia.; Centre for Inflammation, Centenary Institute, The University of Technology Sydney, Sydney, NSW, Australia., Kedzierska K; Department of Microbiology and Immunology, University of Melbourne, Peter Doherty Institute for Infection and Immunity, Parkville, VIC, Australia., Masters SL; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Belz GT; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Binder M; Research Group Dynamics of Early Viral Infection and the Innate Antiviral Response, Division Virus-Associated Carcinogenesis (F170), German Cancer Research Center (DKFZ), Heidelberg, Germany., Hansbro PM; Priority Research Centre for Asthma and Respiratory Diseases, Hunter Medical Research Institute, The University of Newcastle, Newcastle, NSW, Australia.; Centre for Inflammation, Centenary Institute, The University of Technology Sydney, Sydney, NSW, Australia., Nicola NA; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia., Nicholson SE; The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.; Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia.
المصدر:	Immunology and cell biology [Immunol Cell Biol] 2019 Oct; Vol. 97 (9), pp. 840-852. Date of Electronic Publication: 2019 Aug 19.
نوع المنشور:	Journal Article; Research Support, Non-U.S. Gov't
اللغة:	English
بيانات الدورية:	Publisher: Wiley Country of Publication: United States NLM ID: 8706300 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1440-1711 (Electronic) Linking ISSN: 08189641 NLM ISO Abbreviation: Immunol Cell Biol Subsets: MEDLINE
أسماء مطبوعة:	Publication: 2018- : [Hoboken, NJ] : Wiley Original Publication: [Adelaide, South Australia] : University of Adelaide, [c1987-
مواضيع طبية MeSH:	Signal Transduction, Antiviral Agents/metabolism , DEAD Box Protein 58/metabolism , DNA-Binding Proteins/metabolism , Transcription Factors/metabolism , Tripartite Motif Proteins/metabolism , Ubiquitin-Protein Ligases/*metabolism, A549 Cells ; Animals ; Cell Line ; Epithelial Cells/microbiology ; Epithelial Cells/virology ; Gene Deletion ; Humans ; Ligands ; Mice, Inbred C57BL ; RNA/metabolism ; Receptors, Immunologic
مستخلص:	The innate immune system is our first line of defense against viral pathogens. Host cell pattern recognition receptors sense viral components and initiate immune signaling cascades that result in the production of an array of cytokines to combat infection. Retinoic acid-inducible gene-I (RIG-I) is a pattern recognition receptor that recognizes viral RNA and, when activated, results in the production of type I and III interferons (IFNs) and the upregulation of IFN-stimulated genes. Ubiquitination of RIG-I by the E3 ligases tripartite motif-containing 25 (TRIM25) and Riplet is thought to be requisite for RIG-I activation; however, recent studies have questioned the relative importance of these two enzymes for RIG-I signaling. In this study, we show that deletion of Trim25 does not affect the IFN response to either influenza A virus (IAV), influenza B virus, Sendai virus or several RIG-I agonists. This is in contrast to deletion of either Rig-i or Riplet, which completely abrogated RIG-I-dependent IFN responses. This was consistent in both mouse and human cell lines, as well as in normal human bronchial cells. With most of the current TRIM25 literature based on exogenous expression, these findings provide critical evidence that Riplet, and not TRIM25, is required endogenously for the ubiquitination of RIG-I. Despite this, loss of TRIM25 results in greater susceptibility to IAV infection in vivo, suggesting that it may have an alternative role in host antiviral defense. This study refines our understanding of RIG-I signaling in viral infections and will inform future studies in the field. (© 2019 Australian and New Zealand Society for Immunology Inc.)
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فهرسة مساهمة:	Keywords: RIG-I; Riplet; TRIM25; influenza
المشرفين على المادة:	0 (Antiviral Agents) 0 (DNA-Binding Proteins) 0 (Ligands) 0 (Receptors, Immunologic) 0 (Transcription Factors) 0 (Trim25 protein, mouse) 0 (Tripartite Motif Proteins) 63231-63-0 (RNA) EC 2.3.2.27 (RNF135 protein, human) EC 2.3.2.27 (Rnf135 protein, mouse) EC 2.3.2.27 (TRIM25 protein, human) EC 2.3.2.27 (Ubiquitin-Protein Ligases) EC 3.6.1.- (RIGI protein, human) EC 3.6.1.- (Ddx58 protein, mouse) EC 3.6.4.13 (DEAD Box Protein 58)
تواريخ الأحداث:	Date Created: 20190724 Date Completed: 20200417 Latest Revision: 20231213
رمز التحديث:	20240628
DOI:	10.1111/imcb.12284
PMID:	31335993
قاعدة البيانات:	MEDLINE

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تدمد:	1440-1711
DOI:	10.1111/imcb.12284