Fig. 5. CHOP suppresses AKT signaling cascade and promotes JNK/p38 signaling cascades.

a Activation of AKT, JNK, p38, and ERK1/2 signaling cascades during NDV infection. HeLa cells were infected with NDV and harvested at indicted time points. Western blot analysis was performed using antibodies against phospho-AKT, AKT, phospho-JNK, JNK, phospho-p38, p38, phospho-ERK1/2, ERK1/2, NP, and β-actin. The intensities of phospho-AKT, phospho-JNK, phospho-p38, and phospho-ERK1/2 bands were normalized to corresponding total proteins and shown as fold change of NDV (+:−). b, c CHOP regulates the AKT signaling cascades and suppresses MAPK signaling cascades. Cell lysates prepared in Fig. 4b, c were subjected to western blot with indicated antibodies. The intensities of phospho-AKT, phospho-JNK, phospho-p38, and phospho-ERK1/2 bands were normalized to corresponding total proteins, shown as fold change of siCHOP:sic or CHOP:PXJ40F. Results shown are representative of three independent experiments. d The effect of knockdown of AKT, JNK, p38, or ERK1/2 on NDV-induced apoptosis and virus proliferation. HeLa cells were transfected with sic, siAKT, siJNK, sip38, or siERK1/2, then infected with NDV for 20 h. Mock infection was included as control. Cell lysates were analyzed by western blot with indicated antibodies. The intensities of PARP-C and NP were normalized to β-actin and shown as fold change of siTarget:sic. Results shown are representative of three independent experiments.