Abstract: F30V also decreased the percentage of apoptotic cells compared with wild-type (14.8 +- 6.8% versus 19.1 +- 10.1%, p <0.01, without affecting cell-cycle progression) and increased the probability of
HBx-Ser-31 being phosphorylated by PI3K-Akt kinase (known to promote anti-apoptotic activity).
Abstract: CONCLUSIONS:
F30V was closely correlated with HBV-induced
HCC in vivo, reduced HBV replicative efficiency by affecting
HBx-binding to cccDNA and increased anti-apoptotic
HBx activity in vitro.
Abstract: In vitro,
F30V determined a 40% and 60% reduction in pgRNA and
core-associated HBV-DNA compared with wild-type (p <0.05), in parallel with a significant decrease of