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. 2014 Sep 15;111(39):14289–14294. doi: 10.1073/pnas.1407640111

Fig. 6.

Fig. 6.

Foxa3 interferes with CREB-mediated induction of PGC1α expression. (A) Foxa-responsive element adjacent to a CRE-binding site in the PGC1α promoter. (B) Luciferase activity of a WT-PGC1α promoter reporter (PGC1α luc) or of a mutant-PGC1α reporter (PGC1α-mt luc) containing a deletion in the Foxa3-responsive element in cells transiently expressing either vector (Ctrl) or Foxa3, or with knockdown of Foxa3 (siFoxa3), in the presence of vehicle or cAMP. (C) Analysis of PGC1α mRNA levels in differentiated primary cells obtained from BAT and iWAT of 14-mo-old WT (WT, 14m) and Foxa3-null (KO, 14m) mice treated with vehicle or cAMP. (D) Analysis of Foxa3 and CREB occupancy at the PGC1α promoter in brown fat tissues obtained from 2-mo-old (2m) and 14-mo-old (14m) mice by ChIP assay. (E and F) ChIP analysis of CREB (E) and Foxa3 (F) binding at the PGC1α promoter in the presence or absence of cAMP in 10T1/2 cells ectopically expressing either vector (Ctrl) or Foxa3. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01 compared with controls. ##P < 0.01 compared with WT+cAMP.