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. 2022 Aug 15;13(8):707. doi: 10.1038/s41419-022-05101-3

Fig. 4. Synergistic induction of cell death by PKR and the exogenous poly I:C treatment.

Fig. 4

a Schematic representation of PKR and GyrB-PKR fusion proteins and the activation mechanism of GyrB-PKR fusion by coumermycin A1. b Induction of SG by the coumermycin A1 treatment. PKR KO HeLa, GyrB-PKR HeLa, and GyrB-PKR K296H HeLa cells were treated with coumermycin A1 (10 nM for 3 h) and observed for the SG marker TIAR (gray) and G3BP1 (red), as in Fig. 3c. Scale bar = 25 µm. c GyrB-PKR HeLa and GyrB-PKR K296H HeLa cells were mock treated (DMSO) or treated with coumermycin A1 (10 nM) for the indicated times and examined for cell survival. d GyrB-PKR HeLa cells were treated with the indicated chemicals and examined for cell survival at each time point. e GyrB-PKR FK-IPS-1 HeLa cells were treated with the indicated chemicals and examined for cell survival at each time point. Cell survival in (ce) was examined by the Amido black assay (“Materials and methods”) and presented as Amido black intensity (ABI) relative to the mock. Data are represented as the means ± SEM of three independent experiments.