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. 2015 Jan 5;5:659. doi: 10.3389/fimmu.2014.00659

Figure 2.

Figure 2

Enhancement of apoptotic signaling molecules in the presence of BIM-I in TRAIL-stimulated HT1080 cells. (A) Cleavage of PARP, phosphorylation of p38, and concentration of β-actin were determined by western blotting at 0, 30, 60, 120, and 180 min after TRAIL stimulation (200 ng/mL) of HT1080 cells in absence or presence of BIM-I (10 μM). Right panels represent the quantification of fraction of cleaved PARP (top, cleaved PARP/total PARP for each time point) and p38 activation (bottom, relative to maximum value of TRAIL stimulation without BIM-I) using ImageJ (http://imagej.net). (B) Phosphorylation of JNK and levels of cleaved caspase-3 protein were measured by ELISA at 0, 10, 30, 60, 120, and 180 min after TRAIL stimulation (200 ng/mL) of HT1080 cells in the absence or presence of BIM-I (10 μM). Error bars indicate mean values ± SD for n = 3 independent experiments. (C) Schematic representing the mechanism of signaling flux redistribution at p62 pathway junction toward p38 and caspase-3 signaling branches when PKC is inhibited.