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. Author manuscript; available in PMC: 2006 Aug 15.
Published in final edited form as: Mol Cell Endocrinol. 2006 Aug 15;256(1-2):23–33. doi: 10.1016/j.mce.2006.05.005

Fig. 5.

Fig. 5

Ligand-binding PPARβ enhances the dissociation of LXRα-RXRα heterodimers in the mammalian two-hybrid system. (A) HEK293 cells were transfected with 200 ng of GAL4-fused LXRα, VP16-fused RXRα and GAL4DBDx4 TK-luciferase plasmids. TK-luciferase that does not include GAL4DBD (shown as a white bar) and VP16 without RXRα ORF plasmids were used as negative controls. The results are displayed as % values of GAL4-LXRα + TK-luciferase activity. (B) PPARβ and PPARβL405R mutants shown in Fig. 3 were additively transfected using the experimental conditions described in (A) and HEK293 cells were treated without or with 1 μM L-165041. The results were displayed as % values of GAL4-LXRα + VP16-RXRα + GAL4DBDx4 TK-luciferase activity. (C) PPARβ and FXR show a different dose–response for dissociation of LXRα-RXRα heterodimers. PPARβ, FXR and C/EBPα (as a negative control) were additively transfected in a dose dependent manner using the experimental conditions described in (A) and HEK293 cells were treated without or with 1 μM L-165041 or 50 μM chenodeoxycholic acid. The results are displayed as % values of GAL4-LXRα + VP16-RXRα + GAL4DBDx4 TK-luciferase activity. **p < 0.01; ***p < 0.001; NS, no significant difference.