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. 2017 Apr 11;8:576. doi: 10.3389/fmicb.2017.00576

FIGURE 1.

FIGURE 1

Hepatitis C virus (HCV) infection and viral replication reduced GRIM-19 expression. (A,B) Protein levels of GRIM-19 were evaluated using western blot analysis in Huh7 cells infected with HCVcc at days 3, 6, 9, and 12 post-infection (A), FGR cells (B), and SGR cells (B). The relative protein expression was normalized to β-actin as a reference. (C) The endogenous GRIM-19 level was assessed by western blot analysis in Huh7.5.1 cells or Huh7.5.1-derived HCV genotype 3 full genomic replicon cells. The relative protein expression was normalized to β-actin as a reference. (D) Relative levels of endogenous GRIM-19 mRNA in SGR cells, FGR cells, and HCVcc-infected Huh7 cells compared to that in Huh7 cells. β-actin was used as a reference gene. (E) Protein levels of GRIM-19 in liver tissues from patients with chronic liver diseases (CLD) caused by persistent HCV infection (n = 4) were analyzed by western blot analysis. Tissue lysates from liver without viral hepatitis were used as a control (normal; n = 4). β-actin was used as a loading control. The values of the GRIM-19 protein levels were expressed relative to the level in control tissues (right). All data represent the mean ± SEM (n = 3). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared to control.