Skip to main content
. 2014 Aug 14;5(8):e1373. doi: 10.1038/cddis.2014.328

Figure 5.

Figure 5

Omi regulates PGC-1α through GSK3β. (a) Western blotting analysis was performed showing that the knockdown of Omi decreased PGC-1α protein abundance; however, the effects of Omi knockdown were blocked by treatment with SB216763 (5 μM) for 24 h. SHSY-5Y cells were transfected with si-NC or si-Omi, and 24 h after transfection, cells were treated with DMSO or 5 μM SB216763 for another 24 h. Densitometric analyses from three independent experiments were quantified by one-way ANOVA, *P<0.05. (b) Western blotting analysis was performed showing that the knockdown of Omi decreased PGC-1α protein abundance; however, PGC-1α protein abundances were restored when GSK3β was also knockdown. Densitometric analyses from three independent experiments were quantified by one-way ANOVA, *P<0.05. (c) Western blotting analysis was performed showing that PGC-1α protein abundances were decreased in the brains in mnd2 mice; however, PGC-1α protein abundances were increased significantly in SB216763-treated mnd2 mice of 25 days compared with DMSO-treated mnd2 mice. Densitometric analyses from three independent experiments were quantified by one-way ANOVA, *P<0.05. (d) Immunoprecipitation assays showed that the interaction of PGC-1α and Cdc4 was significantly increased in DMSO-treated mnd2 mice as compared with wild-type mice; however, the interaction of PGC-1α and Cdc4 was decreased in mnd2 mice after SB216763 treatment