beta-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection

文献类型： 外文期刊

第一作者： Chang, Long

作者： Chang, Long;Zhu, Liqian;Chang, Long;Zhu, Liqian;Yuan, Weifeng

作者机构：

关键词： BoHV-1; beta-catenin; c-Jun; JNK

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2020 年 248 卷

页码：

收录情况： SCI

摘要： 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-beta-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 beta-catenin and c-Jun in the nucleus was readily detected in virus-infected, but not mock-infected cells. Interestingly, beta-catenin was found to be involved in the regulation of c-Jun signaling in virus-infected cells as iCRT14, a beta-catenin-specific inhibitor that can inhibit beta-catenindependent 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 beta-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 beta-catenin signaling playing in BoHV-1 infection.

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