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

• Published in: Immunology and cell biology Vol. 97; no. 9; p. 840
• Main Authors: Hayman, Thomas J, Hsu, Alan C, Kolesnik, Tatiana B, Dagley, Laura F, Willemsen, Joschka, Tate, Michelle D, Baker, Paul J, Kershaw, Nadia J, Kedzierski, Lukasz, Webb, Andrew I, Wark, Peter A, Kedzierska, Katherine, Masters, Seth L, Belz, Gabrielle T, Binder, Marco, Hansbro, Philip M, Nicola, Nicos A, Nicholson, Sandra E
• Format: Journal Article
• Language: English
• Published: United States 01.10.2019
• Subjects: A549 Cells; Animals; Antiviral Agents - metabolism; Cell Line; DEAD Box Protein 58 - metabolism; DNA-Binding Proteins - metabolism; Epithelial Cells - microbiology; Epithelial Cells - virology; Gene Deletion; Humans; Ligands; Mice, Inbred C57BL; Receptors, Immunologic; RNA - metabolism; Signal Transduction; Transcription Factors - metabolism; Tripartite Motif Proteins - metabolism; Ubiquitin-Protein Ligases - metabolism; influenza; RIG-I; TRIM25; Riplet

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...