{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T09:37:16Z","timestamp":1786441036095,"version":"build-2736575974"},"reference-count":40,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T00:00:00Z","timestamp":1786406400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100006321","name":"National Institutes of Natural Sciences","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006321","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>The innate immune response is the first line of host defense against viral infection. RNA virus infection triggers activation of retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS) signaling pathway, resulting in the formation of prion-like aggregates of MAVS and production of type I interferons (IFN-I). Here, we found that APC7, a subunit of the anaphase-promoting complex\/cyclosome (APC\/C), can significantly restrict the replication of RNA viruses including Enterovirus 71 (EV71) and vesicular stomatitis virus (VSV). Further experiments showed that overexpression of APC7 enhances RNA virus-induced IFN-I expression, whereas knockdown of APC7 reduces it. Moreover, APC7 regulated the innate immune response independently of APC\/C catalytic function. Subsequent analysis indicated that APC7 is partly localized to mitochondria, where it interacts with the transmembrane domain of MAVS. Furthermore, we discovered that APC7 promotes K63-linked polyubiquitination and mitochondrial aggregation of MAVS after RNA virus infection. Taken together, these findings demonstrated that APC7 potentiates the antiviral response through activation of MAVS-mediated signaling, which provides new insights into the regulatory mechanisms of innate immunity and viral infections.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1912055","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T09:11:26Z","timestamp":1786439486000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The APC\/C subunit APC7 exerts antiviral effects by targeting the adaptor protein MAVS"],"prefix":"10.3389","volume":"17","author":[{"given":"Rui","family":"Su","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Henan Medical University","place":["Xinxiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aiping","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Henan Medical University","place":["Xinxiang, China"]},{"name":"Xinxiang Engineering Technology Research Center of Immune Checkpoint Drug for Liver-Intestinal Tumors, Henan Medical University","place":["Xinxiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yifan","family":"Niu","sequence":"additional","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Henan Medical University","place":["Xinxiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiesuo","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Henan Medical University","place":["Xinxiang, China"]},{"name":"Xinxiang Engineering Technology Research Center of Immune Checkpoint Drug for Liver-Intestinal Tumors, Henan Medical University","place":["Xinxiang, 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