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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: Hepatology. 2011 Jul;54(1):229–239. doi: 10.1002/hep.24368

Figure 3. Liver specific deletion of GRP78 exacerbates alcohol-induced ER stress and fatty liver injury.

Figure 3

Figure 3

Comparisons of serum ALT (A), liver triglycerides (B) and cell death (C) between WT and LGKO fed ethanol (WT_E and LGKO_E). Dash lines inside the bars represent levels of pair-fed control. Animals in this group of experiments were 4–6 week old. *p<0.05 and **p<0.01 compared to WT, n=6. (D) TUNEL-stained liver section (×200). (E) Western blots of nuclear protein extracts for activated nSREBP1c and nChREBP, sXbp-1, activated ATF6; C/EBPα using Lamin A/C as loading control, and of whole protein extracts for phosphorylated eIF2α (p-eIF2a) using β-actin as loading control; (F) Diagram depicts impact of Grp78 deletion and ER stress factors on alcohol-induced lipogenesis.