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

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-in

SUBMITTER: Chang L 

PROVIDER: S-EPMC7414362 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature