Skip to main content
. Author manuscript; available in PMC: 2010 Nov 1.
Published in final edited form as: Mol Cell Biochem. 2009 May 15;331(1-2):31–40. doi: 10.1007/s11010-009-0142-1

Figure 1.

Figure 1

Induction of ER stress and cell death by thapsigargin and palmitate in H4IIE liver cells. H4IIE liver cells were incubated for 6 or 16 hours in control media (LG), or control media supplemented with thapsigargin (Thap, 450 nM), oleate (O, 250 µM), or palmitate (P, 250 µM).(A) Real Time PCR analysis of glucose regulated protein 78 (GRP78), growth arrest and DNA damage-inducible gene 34 (GADD34), activating transcription factor 4 (ATF4) and CCAAT/enhancer binding protein homologous protein (CHOP). Data from LG were set to 1. (B) Western blot analysis of GRP78, CHOP and actin (loading control) proteins. The gels shown are representative of five independent experiments and data in graphs are expressed as the ratio of the target protein to actin. (C) ELISA-based cell death and MTT viability assay. Data in graphs are reported as the mean ± SD of triplicate samples from 5 independent experiments. *, significantly (p<0.05) different from LG and O250.