CVB3 is a virulent human pathogen that induces myocarditis and ultimately dilated cardiomyopathy. Although several apoptotic factors are involved in the cell death induced by CVB3, the upstream signal transduction factors of CVB3-induced apoptosis are still unclear. We explored and characterized the role of PKC δ in CVB3-infected cells. PKC δ was cleaved after CVB3 infection and was activated at 6 h postinfection. PKC δ was also translocated into the nucleus via mitochondria after CVB3 infection, and overexpression of wild-type PKC δ reduced the apoptotic cell death caused by CVB3. These results indicate that PKC δ has an anti-apoptotic role in CVB3 infection.
|Number of pages
|Journal of Microbiology and Biotechnology
|Published - Apr 2006
- PKC δ