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. 2016 Feb 1;2:16003. doi: 10.1038/cddiscovery.2016.3

Figure 1.

Figure 1

Defective downregulation of IRES targets and defective induction of secondary necrotic PARP cleavage leads to transformation from blebbishields. (a) TNF-α and TRAIL but not FasL in combination with AZ58 downregulate p70S6K and selected IRES translational targets at 24 h. (b) CHX 10 μg/ml selectively targets c-Myc expression (also see Supplementary Figure S1A). (c) All three death ligands induce similar levels of DNA fragmentation in RT4v6 cells (left bar graph; n=3), but only blebbishields induced by FasL+AZ58 could transform (right bar graph; n=3). (d) Twenty-four hour pulse-chase analysis of timing of degradation of selected IRES translational targets in relation to caspase-3 activation (arrowheads), p70S6K and PARP cleavage (left blot panels), and quantification of apoptotic (89 kDa) and secondary necrotic PARP cleavage (42 kDa) by densitometry (right panels). (e) Schematic representation of lower efficiency of FasL than of TNF-α or TRAIL in combination with AZ58 in downregulating p70S6K and selected IRES targets in relation to secondary necrotic PARP cleavage.