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• W2033651380 endingPage "4920" @default.
• W2033651380 startingPage "4908" @default.
• W2033651380 abstract "ABSTRACT Foot-and-mouth disease virus (FMDV) causes a highly contagious, debilitating disease in cloven-hoofed animals with devastating economic consequences. To survive in the host, FMDV has evolved to antagonize the host type I interferon (IFN) response. Previous studies have reported that the leader proteinase (L pro ) and 3C pro of FMDV are involved in the inhibition of type I IFN production. However, whether the proteins of FMDV can inhibit type I IFN signaling is less well understood. In this study, we first found that 3C pro of FMDV functioned to interfere with the JAK-STAT signaling pathway. Expression of 3C pro significantly reduced the transcript levels of IFN-stimulated genes (ISGs) and IFN-stimulated response element (ISRE) promoter activity. The protein level, tyrosine phosphorylation of STAT1 and STAT2, and their heterodimerization were not affected. However, the nuclear translocation of STAT1/STAT2 was blocked by the 3C pro protein. Further mechanistic studies demonstrated that 3C pro induced proteasome- and caspase-independent protein degradation of karyopherin α1 (KPNA1), the nuclear localization signal receptor for tyrosine-phosphorylated STAT1, but not karyopherin α2, α3, or α4. Finally, we showed that the protease activity of 3C pro contributed to the degradation of KPNA1 and thus blocked STAT1/STAT2 nuclear translocation. Taken together, results of our experiments describe for the first time a novel mechanism by which FMDV evolves to inhibit IFN signaling and counteract host innate antiviral responses. IMPORTANCE We show that 3C pro of FMDV antagonizes the JAK-STAT signaling pathway by blocking STAT1/STAT2 nuclear translocation. Furthermore, 3C pro induces KPNA1 degradation, which is independent of proteasome and caspase pathways. The protease activity of 3C pro contributes to the degradation of KPNA1 and governs the ability of 3C pro to inhibit the JAK-STAT signaling pathway. This study uncovers a novel mechanism evolved by FMDV to antagonize host innate immune responses." @default.
• W2033651380 created "2016-06-24" @default.
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• W2033651380 date "2014-05-01" @default.
• W2033651380 modified "2023-10-10" @default.
• W2033651380 title "3C ^pro of Foot-and-Mouth Disease Virus Antagonizes the Interferon Signaling Pathway by Blocking STAT1/STAT2 Nuclear Translocation" @default.
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• W2033651380 cites W1972089119 @default.
• W2033651380 cites W1978798894 @default.
• W2033651380 cites W1980084515 @default.
• W2033651380 cites W1998762073 @default.
• W2033651380 cites W2001207965 @default.
• W2033651380 cites W2001241809 @default.
• W2033651380 cites W2003043056 @default.
• W2033651380 cites W2006276244 @default.
• W2033651380 cites W2007320083 @default.
• W2033651380 cites W2013519130 @default.
• W2033651380 cites W2017900917 @default.
• W2033651380 cites W2025030639 @default.
• W2033651380 cites W2027334611 @default.
• W2033651380 cites W2029275361 @default.
• W2033651380 cites W2031913105 @default.
• W2033651380 cites W2034649150 @default.
• W2033651380 cites W2039440227 @default.
• W2033651380 cites W2042876447 @default.
• W2033651380 cites W2043188148 @default.
• W2033651380 cites W2043983740 @default.
• W2033651380 cites W2056107229 @default.
• W2033651380 cites W2056142982 @default.
• W2033651380 cites W2059118814 @default.
• W2033651380 cites W2059395206 @default.
• W2033651380 cites W2060065563 @default.
• W2033651380 cites W2060197609 @default.
• W2033651380 cites W2063114480 @default.
• W2033651380 cites W2066293942 @default.
• W2033651380 cites W2071670416 @default.
• W2033651380 cites W2086550292 @default.
• W2033651380 cites W2091978007 @default.
• W2033651380 cites W2092463285 @default.
• W2033651380 cites W2093827911 @default.
• W2033651380 cites W2096372976 @default.
• W2033651380 cites W2102884496 @default.
• W2033651380 cites W2103738533 @default.
• W2033651380 cites W2104707719 @default.
• W2033651380 cites W2106007139 @default.
• W2033651380 cites W2113961792 @default.
• W2033651380 cites W2114174897 @default.
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• W2033651380 cites W2132669016 @default.
• W2033651380 cites W2136920638 @default.
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• W2033651380 cites W2169602184 @default.
• W2033651380 cites W2169853010 @default.
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• W2033651380 doi "https://doi.org/10.1128/jvi.03668-13" @default.
• W2033651380 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3993825" @default.
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• W2033651380 hasPublicationYear "2014" @default.
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