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. 2004 Apr 20;101(17):6570–6575. doi: 10.1073/pnas.0401401101

Fig. 4.

Fig. 4.

A small-molecule inhibitor of Errα inhibits the response to PGC-1α. (A) C2C12 myoblasts transfected with wild-type Errα promoter and the respective expression plasmids were treated with vehicle (0.1% DMSO) or 1 μM XCT790 for 48 h before reporter gene levels were measured. (B) C2C12 cells were transfected with wild-type or Errα-promoter harboring a mutated Errα motif (mutant), together with expression plasmids for Errα, Gabpa, Gabpb1, and PGC-1α. After 48 h, reporter gene levels were determined and normalized to β-galactosidase levels. (C) C2C12 myotubes were infected with GFP- or PGC-1α adenovirus and were treated with vehicle (0.1% DMSO) or 1 μM XCT790 for 1 day. Relative expression levels of several genes were then determined by semiquantitative real-time PCR and were normalized against 18S rRNA levels. (D) Fao rat hepatoma cells were infected with adenoviral GFP or PGC-1α and were treated with vehicle (0.1% DMSO) or 1 μM XCT790 for 1 day before relative gene expression levels were measured by real-time PCR, and were normalized against 18S rRNA levels. *, P < 0.05. NS, not significant.