Rishov Mukhopadhyay, Simeon D. Draganov, Timo Oosenbrug, Jimmy J.L.L. Akkermans, Marjolein Kikkert, Klaus‐Peter Knobeloch, G. Fritz, María Guzmán, Sonia Zúñiga, Robbert Q. Kim, Annemarthe G. van der Veen, Benedikt M. Kessler, Adán Pinto-Fernández, Paul P. Geurink, Ayşegül Sapmaz
The type I Interferon (IFN-I)-induced ubiquitin-like modifier Interferon-Stimulated Gene 15 (ISG15) plays a crucial role in the innate immune response against viral infections. ISG15 is conjugated to target proteins by an enzymatic cascade, called ISGylation. While ubiquitin-specific protease 18 (USP18) serves as the major deISGylase counteracting ISG15 conjugation, ISG15 cross-reactive deubiquitylating enzymes (DUBs) have also been reported. Here, we identify USP24 as an ISG15 cross-reactive DUB through activity-based protein profiling. USP24 processes pro-ISG15 and ISG15-linked substrates in vitro, and its depletion increases ISG15 conjugates following interferon stimulation in cells without altering canonical IFN-I signaling. USP24 knockout cells show increased IFN-β and ISG expression upon activation of cytosolic RNA sensing via viral mimicry. Proteomic analysis identifies RNA helicase Moloney leukemia virus 10 (MOV10) as a specific target of USP24 for deISGylation. Our data revealed that ISGylation of MOV10 promotes MOV10 interaction with IFIT3 and enhances IFN-β production/secretion in response to viral stimuli. This process is negatively regulated by USP24, which directly deISGylates MOV10. Our data highlight USP24's role in modulating ISGylation and IFN-I production, suggesting USP24 as a potential therapeutic agent for infectious and inflammatory diseases.