Fig. 4
From: FGF15 promotes hepatic NPC1L1 degradation in lithogenic diet-fed mice
FGF15-FGFR4 pathway promoted hepatic NPC1L1 protein turnover. The WT and mNPC1L1hepatic-OE mice were fed with 8-week HFCD and LD prior to the indicated experiments. A The serum FGF15 concentrations in WT and mNPC1L1hepatic-OE mice. The hepatic mRNA expression of (B) NPC1L1, and (C) ABCG5/8, CYP7a1, CYP8b1, CYP27a1, CYP7b1 in mNPC1L1hepatic-OE mice. D upper panel: Immunoblot of NPC1L1 and ubiquitin (Ub) from cultured human HepG2 hepatocarcinoma cells, treated with or without FGF19, H3B-6527 and CA. The antibody against tubulin served as the internal control. Lower panel: NPC1L1 ubiquitination was assessed by immunoprecipitating NPC1L1 and immunoblotting using anti-Ub antibody. E Immunoblot of NPC1L1 from cultured human HepG2 hepatocarcinoma cells, treated with or without FGF19 and MG132, with tubulin used as loading controls. The band densities of western blot images were analyzed with the ImageJ software and indicated below the bands, normalized to their loading controls. F The mRNA expression of NPC1L1 in cultured human HepG2 hepatocarcinoma cells, treated with or without FGF19, H3B-6527 and CA. Mann-Whitney U-test for data with non-normal distribution and Student’s t-test for normal distributions. *P < 0.05, **P < 0.01, ns no significance. CA, cholic acid; HFCD, high fat-cholesterol diet; LD, lithogenic diet; Ub, ubiquitination