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. 2018 Aug 10;14(11):1976–1990. doi: 10.1080/15548627.2018.1496877

Figure 2.

Figure 2.

USP14 disrupts DDR signaling in autophagy-deficient cells. (a–c) Confocal immunostaining and graphical representation of γH2AFX and TP53BP1 foci following IR treatment in C4-2 cells co-expressing shATG7 and shUSP14. Nuclei were stained with DAPI. (d–f) Confocal immunostaining and graphical representation of γH2AFX and USP14 foci following IR+/− CQ treatment in C4-2 cells expressing shCtrl and shUSP14. Nuclei were stained with DAPI. Data shown are the means ± SEM (n  =  2); P < 0.05 *, P < 0.01 **. (g) Western blot analysis for USP14 in shCtrl-expressing vs shATG7-expressing C4-2 cells following IR treatment for the indicated time. ACTB/β-actin was used as a loading control. Western blot analysis for USP14 in PC3 cells treated with (h) serum starvation and (i) rapamycin. ACTB/β-actin was used as a loading control.