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. 2022 Dec 22;12:1047177. doi: 10.3389/fonc.2022.1047177

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Copyright © 2022 Guo, Lin, Hua and Wang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TRIM31: Growing influence in innate immunity and autophagy. TRIM31 plays an important role in innate immunity; TRIM31 interacts with MAVS and catalyzes the Lys63 (K63)-linked polyubiquitination of MAVS to promote the formation of prion-like MAVS aggregates after viral infection. USP18 promotes TRIM31-mediated K63-linked MAVS polyubiquitination, while PB1-F2, Rac1, PRMT7, SARS2-NP and FAF1 inhibit TRIM31-mediated K63-linked MAVS polyubiquitination. TRIM31 directly binds to NLRP3 and promotes K48-linked polyubiquitination and proteasomal degradation of NLRP3. AKT and CRNDE decreased TRIM31-mediated NLRP3 ubiquitination. Alongside its emerging role in innate immunity, TRIM31 is also known to be involved in autophagy.