Supplementary Figures 1-9, Supplementary Tables 1-3 from An Integrated Stress Response Agent that Modulates DR5-Dependent TRAIL Synergy Reduces Patient-Derived Glioma Stem Cell Viability

S1: Raw bioluminescence data obtained from screens of kinase, protease, and redox inhibitors. S2: Bioluminescent and viability data from U251 DR5 Luciferase cells treated with an NH125 dilution series. S3: Representative images of T4213 neurospheres taken under 40X magnification demonstrate that T4213 enrich for CD133 (red) SOX2 (orange) and Nestin (green) (scale bar = 25 microns). S4: Representative phase contrast images of TMZ, and NH125 treated GSC taken under 10X magnification (scale bar = 100 microns). S5: Caspase 3/7 activity increases in NH125 treated GSC. GSC were incubated with either 0 M NH125 (0.1% DMSO) or 5 M NH125 for twenty-four hours followed by addition of Caspase 3/7 Glo. S6: NH125 leads to a dose dependent increase in markers of apoptosis. S7: GSC that acquire a differentiated morphology are less sensitive to NH125. S8: The ten most significant canonical pathways from analysis of the transcriptional data of NH125 treated U251 and NHA. S9: PEG-PCL-NH125 treatment of U251 leads to an increase in CHOP and DR5 expression in vitro. Table S1: Knockout of CHOP leads to an abrogation of NH125 mediated TRAIL synergy. Table S2: IC50 values from a panel of NH125 treated cells. Table S3: Addition of low dose TRAIL leads to increased synergy in glioma stem cells.