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Upon viral infection, MAVS forms prion\u2010like aggregates to activate NF\u2010\u03baB and IRF3, thereby inducing type I interferon production and antiviral responses. Here, we identify RNA\u2010binding motif protein 6 (RBM6) as a previously unrecognized positive regulator of MAVS signaling during Sendai virus (SeV) infection. RBM6 overexpression enhanced SeV\u2010induced IFN\u2010\u03b2 expression, whereas RBM6 deficiency impaired this response. Mechanistically, RBM6 enhanced K63\u2010linked polyubiquitination of MAVS, promoting MAVS aggregation and facilitating the recruitment of TRAF6. Domain\u2010mapping analysis further localized the antiviral activity of RBM6 to its zinc finger (ZnF) domain spanning residues 850\u20131045. Together, these findings establish RBM6 as an important enhancer of MAVS signalosome assembly and provide new insight into ubiquitin\u2010dependent regulation of the RLR antiviral pathway.<\/jats:p>","DOI":"10.1002\/jmv.71173","type":"journal-article","created":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T11:21:52Z","timestamp":1791026512000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["RBM6 Facilitates RLR\u2010Mediated Antiviral Responses by Promoting K63\u2010Linked Ubiquitination of MAVS"],"prefix":"10.1002","volume":"98","author":[{"given":"De\u2010Ping","family":"Kong","sequence":"first","affiliation":[{"name":"College of Life Science Jiangxi Normal University Nanchang Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ni","family":"Zhong","sequence":"additional","affiliation":[{"name":"College of Life Science Jiangxi Normal University Nanchang Jiangxi 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