Suppression of Actinomycin D-Induced Apoptosis by the NS3 Protein of Hepatitis C Virus ☆

摘要: Abstract The NS3 protein of hepatitis C virus is a multifunctional that indispensable for replication. Little known, however, about the possible effects on host cell function(s). In present study, we demonstrated NIH3T3 cells constitutively expressing carboxy-terminally truncated (NS3ΔC) were more resistant to actinomycin D-induced apoptosis than control cells. We also observed induction p53 expression by D treatment was weaker in NS3ΔC-expressing However, WAF1 same not different between two groups. Taken together, our results suggest possibility NS3ΔC suppressed through at least partly, if solely, p53-dependent, WAF1-independent pathway.