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• W3048016738 endingPage "108804" @default.
• W3048016738 startingPage "108804" @default.
• W3048016738 abstract "C-Jun, activated by various extracellular signals, is important for cell differentiation, proliferation, apoptosis, and inflammatory responses. We have previously reported that bovine herpesvirus 1 (BoHV-1) infection in MDBK cells stimulates the c-Jun NH2-terminal kinase (JNK)/c-Jun cascade for efficient replication. However, the mechanisms regarding the regulation of c-Jun following BoHV-1 infection remain unknown. In this study, we show that virus infection increases accumulation of p-c-Jun(S73) (phosphorylated c-Jun at Ser73) and p-β-catenin(S552) in the nucleus, resulting in relocalized nuclear p-c-Jun(S73) to assemble in highlighted punctum via a confocal microscope assay. An association between β-catenin and c-Jun in the nucleus was readily detected in virus-infected, but not mock-infected cells. Interestingly, β-catenin was found to be involved in the regulation of c-Jun signaling in virus-infected cells as iCRT14, a β-catenin-specific inhibitor that can inhibit β-catenin-dependent transcriptional activity, was able to decrease protein expression and phosphorylation of c-Jun. Furthermore, we suggest that BoHV-1 infection stimulates c-Jun phosphorylation regulated by β-catenin via both c-Jun NH2-terminal kinase (JNK)-dependent and JNK-independent mechanisms. These data add to our knowledge regarding the regulation of c-Jun following virus infection and further support the important roles of β-catenin signaling playing in BoHV-1 infection." @default.
• W3048016738 created "2020-08-13" @default.
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• W3048016738 date "2020-09-01" @default.
• W3048016738 modified "2023-10-14" @default.
• W3048016738 title "β-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection" @default.
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• W3048016738 doi "https://doi.org/10.1016/j.vetmic.2020.108804" @default.
• W3048016738 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7414362" @default.
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