Fig. 5.

Yap-dependent proliferation in livers with impaired autophagy is potentially druggable. a Controls (Atg7^F/F) and Atg7 KO (Alb-CRE:Atg7^F/F) mice were treated for 21 days with either Yap/Tead inhibitor verteporfin or vehicle. N = 4 per group. VP, verteporfin; Veh, vehicle. b Immunostaining for Ki67 in liver sections from control and Atg7 KO mice treated with either verteporfin or vehicle. Scale bar 100 µm. Large inserts are enlargements of small inserts. c Quantitation of Ki67⁺ nuclei per 100x field per mouse treated with either verteporfin or vehicle. Ten 100x fields per mouse were analyzed. d qRT-PCR analysis of whole liver RNA from control and Atg7 KO mice, treated with verteporfin or vehicle. Cyr61 mRNA expression was normalized to Gapdh expression and then normalized to control animals. Data from two independent experiments. e [³H]-thymidine incorporation assay in scram- and shAtg7-AML12 cells after incubation with verteporfin or vehicle. Data from three independent experiments, measurements in triplicates. ****P = 0.0003. f Tead4-Luciferase assay of scram- and shAtg7-infected AML12 cells after incubation with verteporfin or vehicle. Data from two independent experiments Data represent mean ± SD. P-values analyzed by two-way ANOVA and Tukey’s HSD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 unless indicated otherwise. ns, not significant; VP, verteporfin; Veh, vehicle