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. 2020 Jun 19;11(12):894–914. doi: 10.1007/s13238-020-00734-6

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic depiction of the proposed role of TRIM35 in antiviral immunity against IAV infection. TRIM35, TRAF3, and IAV PB2 form a circuit in which two means are employed by TRIM35 to defend the host against IAV infection. TRIM35 catalyzes K63-linked polyubiquitination of TRAF3 and activates RIG-I antiviral signaling; although IAV PB2 prevents K63-linked polyubiquitination of TRAF3, TRIM35 directly mediates K48-linked polyubiquitination and degradation of IAV PB2