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. Author manuscript; available in PMC: 2017 Apr 19.
Published in final edited form as: Cell Metab. 2013 May 7;17(5):685–694. doi: 10.1016/j.cmet.2013.03.016

Figure 5. PGC-1’s suppressive effect requires active PPARγ and involves SIRT1-mediated deacetylation.

Figure 5

(A) Opposing effects of rosiglitazone and GW9662 on BACE1 expression levels. Western blot analysis was conducted at 6 hr after treatment in neurons. (B) PGC-1α effect is dependent on active PPARγ but not on its ligand. Rosiglitazone or GW9662 compounds were added to the HEK293 cells 24 hr after transfection with PGC-1α plasmid and BACE1 gene transcription was determined 6h later by qRT-PCR. Data are represented as means ± S.D. from 3 independent experiments with * indicating P< 0.05. (C) Acetylation status of PPARγ, PGC-1α and PGC-1β was determined by Western. (D) PPARγ represses BACE1 in its active, non-acetylated form. Various plasmids were transfected, alone or in combination, into HEK293 cells and BACE1 qRT-PCR was conducted 24 hr later. For panels C and D, data are represented as means ± S.D. from 3 independent experiments with * indicating P< 0.05 and ** indicating P<0.01. “n.s.” indicates non-statistically significant.