The assessment of <i>src</i>, p-ERK and p-AKT signaling in wild-type, p53 mutant and Tg(<i>l-fabp</i>:HBx-mCherry;<i>cmcl2</i>:GFP) fish with different liver diseases.

<p>(A) Immunohistochemical analysis of <i>src</i> protein expression in hepatocytes from the GFP-mC and p53 mutant control fish and HBx(p53^-) transgenic fish at 11 months. (B) src IHC results from HBx transgenic fish at 1.5, 7, 9 and 11 months. (C) src IHC results from HBx(p53^-) transgenic fish at 1.5, 7, 9 and 11 months. (D) Immunohistochemical detection of phosphorylated ERK and phosphorylated AKT in 11-month-old Tg(<i>l-fabp</i>:HBx-mCherry;<i>cmcl2</i>:GFP) transgenic fish with hyperplasia and HCC (x 400). Scale bars: 50 μm. (E) Western blot analysis for the activation of erk and akt in the livers of transgenic fish at different stages of HCC development. After measuring the band intensity using the UVP VisionWorks LS software, the relative density was normalized to β–actin. The ratios of p-erk/erk and p-akt/akt were analyzed, and the data are expressed as fold changes of HBx(p53^-) transgenic fish relative to GFP-mC controls.