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. 2022 Oct 7;58(10):1411. doi: 10.3390/medicina58101411

Figure 3.

Figure 3

The effect of co-culturing with C1R, C1R-B*2704 C67S, or C1R-B*2704 cells on the PI3K/AKT signaling of NK-92MI cells. (A) Analysis of the PI3K/AKT signaling in NK-92MI cells induced by co-culturing with C1R, C1R-B*2704 C67S, or C1R-B*2704 cells by using Western blotting. An aliquot (50 μg) of crude proteins extracted from NK-92MI cells after co-culturing with C1R, C1R-B*2704 C67S, or C1R-B*2704 cells was separated with SDS-PAGE, analyzed via Western blotting, and probed for phospho-AKT, AKT, and actin. (B) The ratio of phospho-AKT/actin averaged from four independent experiments in Figure 3A is plotted. The ratio of phospho-AKT/actin obtained from NK-92MI cells co-cultured with C1R cells was set to one. (C) The induced PI3K/AKT pathway of NK-92MI cells co-cultured with C1R-B*2704 cells was blocked by the PI3K inhibitor. (D) The ratio of phospho-AKT/actin averaged from four independent experiments in Figure 3C is plotted. (E) The perforin expression of NK-92MI cells co-cultured with C1R-B*2704 was suppressed by treatment with the PI3K inhibitor. (F) The ratio of perforin/actin averaged from four independent experiments in Figure 3E is plotted.