Skip to main content
. 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. 4.

Fig. 4

RXRα expression attenuates repression of the angptl3 promoter by PPARβ. Two reporter genes were used: (A) PPRE-TK as shown in Fig. 3C, and (B) the angptl3 promoter (D4 mutant as shown in Fig. 2A). The amount (μg) of RXRα plasmid is shown in the figure (0.2 or 0.5 μg). (C) RXRα with a low heterodimerization potential with PPARs has impaired attenuation of the angptl3 promoter. RXRαY397A and RXRαK417A were characterized in an earlier report (Vivat-Hannah et al., 2003). The amount of RXRα, RXRαY397A and RXRαK417A added was 0.05 μg. The D4 mutant of the angptl3 promoter was used as a reporter plasmid. The results are displayed as % values of control without PPARβ vector. (D) PPAPβ has no effect on the transcriptional activity of the GAL4-fused LXRα. HepG2 cells were transfected with the GAL4DBDx4 TK-luciferase and GAL4-fused LXRα plasmids without or with PPARβ and cells were treated without or with 1 μM L-165041 and 100 nM T0901317. TK-luciferase that does not include GAL4DBD (shown as white bar) and GAL4 plasmids, were used as negative control. *p < 0.05; ***p < 0.001; NS, no significant difference.