Fig. 5

Loss of BOK induces p19^INK4d and p21^cip1 expression. a Quantitative western blot analysis of p19^INK4d expression using near-infrared fluorescence of liver extracts from WT and Bok^-/- animals treated with DEN (100 mg/kg BW). Values represent the mean ± SD (n = 4 mice per group). b Immunohistochemistry of liver sections showing cytoplasmic and nuclear localization of p19^INK4d in untreated WT animals and predominantly nuclear localization in Bok^-/- livers. c Immunohistochemistry of liver sections indicating p19^INK4d staining (red) in tumors from WT and Bok^-/- animals. Counterstain was performed with Mayer’s Hematoxilin. d Quantitative western blot analysis using near-infrared fluorescence of p21^cip1 expression of liver extracts from WT and Bok^-/- animals treated with DEN (100 mg/kg BW). Values represent the mean ± SD (n = 4 mice per group). e Immunohistochemistry of liver sections showing negative staining for p21^cip1 in untreated WT animals and predominantly nuclear localization in Bok^-/- mice (red). f Immunohistochemistry of liver sections indicating p21^cip1 negative staining in tumors from WT mice and positive staining for Bok^-/- tumors (red). T tumor area, NT non-tumor area. At least two tumors/animal and 3–4 animals per genotype were used for quantifications in (c) and (f)