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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Hepatology. 2012 Apr 23;55(6):1942–1953. doi: 10.1002/hep.25594

Fig. 2. Binding of PPARγ to MAT2A PPRE sites.

Fig. 2

A. Control and RSG-treated BSC cells were subjected to ChIP to measure the binding of PPARγ to the MAT2A PPRE sites as described under “Experimental procedures”. Input genomic DNA (Input) was used as the loading control and immunoprecipitation with a GFP antibody was used as a negative control. Results are representative agarose gel images of three experiments in duplicates. B. Genomic DNA from immunoprecipitated chromatin as in ‘A’ was quantitated by ChIP real-time PCR as described under “Experimental procedures”. The differential target site occupancy of PPARγ on MAT2A was normalized to input genomic DNA and expressed as fold over control. Results represent mean ± S.E. from three experiments in duplicates. *P<0.005, **P<0.05 vs. control. C. The binding of PPARγ to MAT2A PPREs from BDL HSCs and sham controls was assessed as described in ‘A’. Representative agarose gel images from five HSC preparations in duplicates are shown. D. Genomic DNA from immunoprecipitated chromatin described in ‘C’ was quantitated by ChIP real-time PCR as described under “Experimental procedures”. The differential target site occupancy of PPARγ on MAT2A was normalized to input genomic DNA and expressed as fold over sham. Results represent mean ± S.E. from five HSC preparations in duplicates. *P<0.005 vs. sham.