Fig. 5: Increased sensitivity of PME-1 overexpressing GBM cells to oxidative stress correlates with increased RIPK1 phosphorylation, and is inhibited by necrostatin-1 but not by a pan-caspase inhibitor. | Cell Death Discovery

Fig. 5: Increased sensitivity of PME-1 overexpressing GBM cells to oxidative stress correlates with increased RIPK1 phosphorylation, and is inhibited by necrostatin-1 but not by a pan-caspase inhibitor.

From: PME-1 sensitizes glioblastoma cells to oxidative stress-induced cell death by attenuating PP2A-B55α-mediated inactivation of MAPKAPK2-RIPK1 signaling

Fig. 5

A Representative Western blots of phospho-RIPK1 and total RIPK1 levels in U87MG PME-1-GFP cells after treatment with 2.5 mM H2O2 for the indicated duration. B Quantification of phospho-RIPK1/total RIPK1 shown in panel A (N = 3, two-way ANOVA). C Sensitivity of U87MG PME-1-GFP cells to 16 h t-BHP treatment (different concentrations) with or without 8 h pretreatment with 100 μM necrostatin-1, as determined by MTT (N = 4, statistical significance is shown in Fig. S3A). D Sensitivity of U87MG PME-1-GFP cells to 16 h t-BHP treatment (different concentrations) with or without 8 h pretreatment with 100 μM Z-VAD-FMK, as determined by MTT (N = 4, statistical significance is shown in Fig. S3B).

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