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. Author manuscript; available in PMC: 2014 Sep 26.
Published in final edited form as: Sci Signal. 2013 Sep 3;6(291):ra77. doi: 10.1126/scisignal.2004060

Fig. 1. Deletion of Amot attenuates oval cell proliferation and tumorigenesis induced by DDC treatment or Nf2KO in the liver.

Fig. 1

(A) Immunofluorescence (IF) analysis of CK19 abundance in liver sections from untreated or DDC-treated wild-type (WT) (Ctrl) or AmotKO mice. Representative images of CK19-stained livers from each experimental group are shown. Oval cell response is shown as mean ± SEM of CK19+ cells per portal track (two portal tracks per animal, n = 5 mice). *P = 0.02; **P = 2 × 10−5, analysis of variance (ANOVA) with Bonferroni correction. One-month-old DDC experimental groups: Ctrl/–DDC (n = 3 mice), Ctrl/+DDC (n = 4), AmotKO/+DDC (n = 6). Four-month-old DDC experimental groups: Ctrl/+DDC (n = 5), AmotKO/+DDC (n = 5). P.V., portal vein. Scale bar, 50 µm (B) Percentage of liver weight to body weight in control (Ctrl; n = 20 mice), AmotKO (n = 10), Nf2KO (n = 8), and DKO (n = 17) mice at 7 weeks of age. *P = 0.02; ***P < 0.001, ANOVA with Bonferroni correction. (C) Percentage and ratio of tumor-free WT (Ctrl; n = 20 mice), AmotKO (n = 10), Nf2KO (n = 8), and DKO (n = 17) mice. (D) Immunohistochemistry (IHC) analysis of CK19 abundance in livers from WT (Ctrl), AmotKO, Nf2KO, and DKO mice. Representative images of CK19-stained livers from each experimental group are shown. Scale bar, 100 µm. (E) Analysis of (D). Data are means ± SEM of CK19+ cells per portal track in the nontumor regions of the livers from each genotype. WT (Ctrl; n = 5 mice), AmotKO (n = 3), Nf2KO (n = 4), and DKO (n = 5). **P = 0.024; ***P < 0.001, two-tailed t test.