title: MAVS Coordination of Antiviral Innate Immunity.
abstract: RNA virus infection is sensed in the cytoplasm by the retinoic acid-inducible gene I (RIG-I)-like receptors. These proteins signal through the host adaptor protein MAVS to trigger the antiviral innate immune response. Here, we describe how MAVS subcellular localization impacts its function and the regulation underlying MAVS signaling. We propose a model to describe how the coordination of MAVS functions at the interface between the mitochondria and the mitochondrion-associated endoplasmic reticulum (ER) membrane programs antiviral signaling.
authors.affiliation: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA.
authors.forename: Christine
authors.initials: C
authors.lastname: Vazquez
authors.affiliation: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA stacy.horner@duke.edu.
authors.forename: Stacy M
authors.initials: SM
authors.lastname: Horner
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D054884:Host-Pathogen Interactions; D007113:Immunity, Innate; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D012328:RNA Viruses / Q000276:immunology*; D015398:Signal Transduction
chemical_list: D048868:Adaptor Proteins, Signal Transducing