Figure 7From: BIMELis a key effector molecule in oxidative stress-mediated apoptosis in acute myeloid leukemia cells when combined with arsenic trioxide and buthionine sulfoximine BSO triggers phosphorylation of MCL1and BIM EL via activation of JNK. A, The phosphorylation of JNK, ERK1/2 and p38 was determined by immunoblotting. HL60 cells were treated with ATO/BSO or ATO in the presence or absence of NAC or DTT for 12 h. B, The phosphorylation of BIMEL and MCL1, and the cleavage of caspase 3 and PARP, were determined by immunoblotting. HL60 cells were treated with ATO/BSO or ATO in the presence of SP600125 (10 μM) as a JNK inhibitor, U0126 (2 μM) as an ERK1/2 inhibitor, or SB203580 (10 μM) as a p38 inhibitor, PD035901 (100 nM)as a MEK1/2 inhibitor for 12 h. A typical result of 3 independent experiments is shown.Back to article page