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• W2927409568 abstract "The arterivirus nsp4-encoded 3C-like protease (3CL pro ) plays an important role in virus replication and immune evasion, making it an attractive target for antiviral therapeutics. Previous work suggested that PRRSV nsp4 suppresses type I IFN production by cleaving NEMO at a single site. In contrast, the present study demonstrates that both EAV and PRRSV nsp4 cleave NEMO at multiple sites and that this strategy is essential for disruption of type I IFN production. Moreover, we reveal that EAV nsp4 also cleaves NEMO at glutamine 205 (Q205), which is not targeted by PRRSV nsp4. Notably, targeting a glutamine in NEMO for cleavage has been observed only with picornavirus 3C proteases (3C pro ) and coronavirus 3CL pro . In aggregate, our work expands knowledge of the innate immune evasion mechanisms associated with NEMO cleavage by arterivirus nsp4 and describes a novel substrate recognition characteristic of EAV nsp4." @default.
• W2927409568 created "2019-04-11" @default.
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• W2927409568 date "2019-06-15" @default.
• W2927409568 modified "2023-09-27" @default.
• W2927409568 title "Arterivirus nsp4 Antagonizes Interferon Beta Production by Proteolytically Cleaving NEMO at Multiple Sites" @default.
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• W2927409568 doi "https://doi.org/10.1128/jvi.00385-19" @default.
• W2927409568 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6613749" @default.
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