Figure 3: PPARγ controls HK2 and PKM2 expression in PTEN-null liver.
From: PPARγ contributes to PKM2 and HK2 expression in fatty liver
(a) Immunoblot analysis of protein expression in liver and WAT tissue of WT mice. (b) RT–QPCR analysis of relative transcript levels of PPARγ in the mouse livers of indicated genotypes. Data are mean ±s.e.m., n=5 (P<0.05 (a) versus WT; (b) versus AlbCre;PTENf/f, 2-tailed, unpaired Student's t test). (c) Immunoblot analysis showing levels of PPARγ in liver nuclear extracts. The ratio to TATA-binding nuclear protein of the densitometric assay ±s.e.m. is presented, n=4–5 (P<0.05 (a) versus WT; (b) versus AlbCre;PTENf/f, 2-tailed, unpaired Student's t test). (d) Relative transcript levels of CD36 and CIDE-C in the mouse livers of indicated genotypes. Data are mean ±s.e.m., n=7 (P<0.05 (a) versus WT; (b) versus AlbCre;PTENf/f; 2-tailed, unpaired Student's t test). (e) Endogenous PPARγ chromatin immunoprecipitation assessed for CD36, PKM2 and HK2 murine promoters relative to immunoprecipitation with nonspecific IgG. Data are presented as an average of fold induction over WT control mice of two independent experiments, n=4.
