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. 2013 May 28;8(5):e64256. doi: 10.1371/journal.pone.0064256

Figure 1. IRAK2 knock down selectively inhibits ER stress-induced cell death.

Figure 1

(a) Hits identified by siRNA kinome library screening after treatment of PPC1 cells with CDDO-Im for 24 hrs. Representative data are shown from an assay plate. Cell viability was estimated by measuring cellular ATP levels (% relative to untreated control). Asterisks represent the hits obtained with IRAK2 siRNAs. Caspase 8 siRNAs were employed as positive controls and scrambled RNAs as negative controls. (b) PPC1 were transfected with scrambled (SC) or 3 independent siRNAs targeting IRAK2 or Caspase 8 (positive control) then treated with CDDO-Im (1 µM) for 3 hrs. Cells were then lysed and Caspase 3/7 activity as measured. Data are expressed as fold induction from the control. Data are mean ± std dev (SD), n = 3. (c) IRAK2 siRNA Knockdown was verified by measuring IRAK2 mRNA expression by qRT-PCR. Data are mean ± SD, n = 3. (d) IRAK2 is selectively involved in ER stress-induced cell death. PPC1 cells were transfected two siRNAs targeting IRAK2 or with scrambled (SC) control siRNA. After 1 day, cells were cultured without (black bars) or with Thapsigargin (TG), TNF-α+cycloheximide, or Staurosporine (STS) (white bars) for 24 hrs. Cell viability was estimated by measuring ATP levels, expressing data as % of control untreated cells (mean±SD, n = 3).