{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["104(35)"],"submitter":["Jounai N"],"pubmed_abstract":["Autophagy is an essential process for physiological homeostasis, but its role in viral infection is only beginning to be elucidated. We show here that the Atg5-Atg12 conjugate, a key regulator of the autophagic process, plays an important role in innate antiviral immune responses. Atg5-deficient mouse embryonic fibroblasts (MEFs) were resistant to vesicular stomatitis virus replication, which was largely due to hyperproduction of type I interferons in response to immunostimulatory RNA (isRNA), such as virus-derived, double-stranded, or 5'-phosphorylated RNA. Similar hyperresponse to isRNA was also observed in Atg7-deficient MEFs, in which Atg5-Atg12 conjugation is impaired. Overexpression of Atg5 or Atg12 resulted in Atg5-Atg12 conjugate formation and suppression of isRNA-mediated signalin"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pagination":["14050-5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1955809"],"repository":["biostudies-literature"],"pubmed_title":["The Atg5 Atg12 conjugate associates with innate antiviral immune responses."],"pmcid":["PMC1955809"],"pubmed_authors":["Miyawaki A","Takeshita F","Sawano A","Ishii KJ","Okuda K","Kobiyama K","Jounai N","Kawai T","Akira S","Suzuki K","Xin KQ"],"additional_accession":[]},"is_claimable":false,"name":"The Atg5 Atg12 conjugate associates with innate antiviral immune responses.","description":"Autophagy is an essential process for physiological homeostasis, but its role in viral infection is only beginning to be elucidated. We show here that the Atg5-Atg12 conjugate, a key regulator of the autophagic process, plays an important role in innate antiviral immune responses. Atg5-deficient mouse embryonic fibroblasts (MEFs) were resistant to vesicular stomatitis virus replication, which was largely due to hyperproduction of type I interferons in response to immunostimulatory RNA (isRNA), such as virus-derived, double-stranded, or 5'-phosphorylated RNA. Similar hyperresponse to isRNA was also observed in Atg7-deficient MEFs, in which Atg5-Atg12 conjugation is impaired. Overexpression of Atg5 or Atg12 resulted in Atg5-Atg12 conjugate formation and suppression of isRNA-mediated signalin","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Aug","modification":"2026-07-15T11:26:59.169Z","creation":"2025-08-31T03:08:47.065Z"},"accession":"S-EPMC1955809","cross_references":{"pubmed":["17709747"],"doi":["10.1073/pnas.0704014104"]}}