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. 2005 Feb 15;19(4):453–461. doi: 10.1101/gad.1263305

Figure 1.

Figure 1.

Identification of a functional PPRE in the GyK gene. (A) Luciferase reporter assays of transiently transfected 3T3-L1 adipocytes using different truncations of the GyK enhancer/promoter in the pGL2 plasmid vector treated with vehicle (DMSO) or rosiglitazone (rosi). (*) p < 0.01 vs. vehicle. (B) Alignment of mouse, rat, and human GyK, aP2, PEPCK, and perfect DR-1 PPRE region. (C) DNA mobility-shift assay using a 32P-labeled fragment from the GyK enhancer (–2041 to –1886 bp). Competition using cold oligonucleotides containing the GyK, aP2, or ideal DR-1 PPREs, or mutant forms, at 10- and 50-fold molar excess is shown at right. Mutation of the PPARγ/RXRα-binding site in the GyK gene abolishes rosiglitazone induction in adipocytes. (P/R) PPARγ/RXRα heterodimer complex; (FP) free probe. (D) Luciferase assay of the GyK reporter plasmid (–2009 in Fig. 2A) with (WT) or without (Mut1) the PPRE Mut 1 shown in Figure 2B. (*) p < 0.001 vs. vehicle; (#) p < 0.01 vs. wild type treated with vehicle. (RLU) Relative luciferase units.