<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>104(35)</volume><submitter>Jounai N</submitter><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</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pagination>14050-5</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1955809</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Atg5 Atg12 conjugate associates with innate antiviral immune responses.</pubmed_title><pmcid>PMC1955809</pmcid><pubmed_authors>Miyawaki A</pubmed_authors><pubmed_authors>Takeshita F</pubmed_authors><pubmed_authors>Sawano A</pubmed_authors><pubmed_authors>Ishii KJ</pubmed_authors><pubmed_authors>Okuda K</pubmed_authors><pubmed_authors>Kobiyama K</pubmed_authors><pubmed_authors>Jounai N</pubmed_authors><pubmed_authors>Kawai T</pubmed_authors><pubmed_authors>Akira S</pubmed_authors><pubmed_authors>Suzuki K</pubmed_authors><pubmed_authors>Xin KQ</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Atg5 Atg12 conjugate associates with innate antiviral immune responses.</name><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</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Aug</publication><modification>2026-07-15T11:26:59.169Z</modification><creation>2025-08-31T03:08:47.065Z</creation></dates><accession>S-EPMC1955809</accession><cross_references><pubmed>17709747</pubmed><doi>10.1073/pnas.0704014104</doi></cross_references></HashMap>