Fig. 6

PPAR induction of the spotted gar fabp1 promoter was PPARα- and PPARγ-selective. a,b) Firefly luciferase activity driven by the fapb1 promoter normalized to Renilla luciferase activity driven by the TK promoter in HEK293A cells treated with 1 nM – 10 μM WY14643 (PPARα agonist) (a) or rosiglitazone (PPARγ agonist) (b) ± 240 nM GW6471 (PPARα antagonist) or 10 nM T0070907 (PPARγ antagonist) for 24 h. C) Site-directed mutagenesis was used to alter the DR1 PPAR binding sites of two fabp1 PPREs at −1,953 bp (ΔPPRE-1) or −539 bp (ΔPPRE-2). d, e) Firefly luciferase activity driven by the fapb1 ‘No mutation’, ΔPPRE-1, or ΔPPRE-2 promoters normalized to Renilla luciferase activity driven by the TK promoter in HEK293A cells treated with 1 nM – 10 μM WY14643 (d) or rosiglitazone (e). Data are mean ± SD. *P < 0.001 compared to agonist alone or ‘No mutation’, as determined via two-way ANOVA followed by Bonferroni’s post-hoc test. n = 3 – 4