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. 2012 Jun 15;26(12):1300–1305. doi: 10.1101/gad.192856.112

Figure 4.

Figure 4.

VP suppressed liver overgrowth caused by YAP overexpression or inactivation of Nf2. (A) Experimental design. Three-week-old YAP transgenic mice were fed 20 mg/L Dox for 8 d. VP suspension (100 mg/kg) was administered by intraperitoneal injection once every other day during the 8-d period. (B) Livers from control (Dox+DMSO; left picture) and VP-treated (Dox+VP; right picture) YAP transgenic mice (left) and quantification of liver-to-body weight ratio (right) at the end of the 8-d period. The VP-treated mice had significantly smaller livers than control livers (7.3% vs. 8.9%, n = 5 in each group, P < 0.001, t-test). (C) Phospho-H3 (PH3) staining of liver sections (left) and quantification of PH3-positive cells (right) of liver sections from B. (D) Experimental design. Timed pregnant Nf2flox2/flox2 mothers (after mating with Alb-Cre; Nf2flox2/flox2 males) received intraperitoneal injection of VP (100 mg/kg) or DMSO every other day starting at 9 d after detection of vaginal plugs (corresponding to E9.5 for embryos carried by the pregnant mothers). Newborn pups (corresponding to E18.5) were analyzed for liver phenotypes. (E) CK staining of liver sections from E18.5 Alb-Cre; Nf2flox2/flox2 pups that had been subjected to control (DMSO) (left) or VP (right) treatment from E9.5 to E18.5. The graph shows quantification of CK-positive BECs.