Endoplasmic Reticulum Stress Mediated MDRV p10.8 Protein-Induced Cell Cycle Arrest and Apoptosis Through the PERK/eIF2α Pathway.

ABSTRACT: In this study, the mechanism of Muscovy duck reovirus (MDRV) p10.8 protein-induced pathogenesis was investigated, with a focus on endoplasmic reticulum (ER) stress. In chicken embryo fibroblasts cell lines (DF1), pCI-neo-flg-p10.8 protein transfection increased the phosphorylation (p-) levels of PERK and eIF2α as shown by Western blotting analysis and led to the dissociation of BiP from PERK as shown by co-immunoprecipitation (Co-IP) analysis. Results of treatment with both ER stress activator and inhibitor further confirmed that p10.8 protein induced ER stress. Subsequently, using flow cytometry analysis, it was also found that p10.8 protein induced cell cycle arrest during the G0/G1 phase. Furthermore, p10.8 transfection increased the phosphorylation levels of PERK and eIF2α, and reduced

SUBMITTER: Wang Q 

PROVIDER: S-EPMC6021497 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature