Deactivation of peroxisome proliferator–activated receptor-α during cardiac hypertrophic growth
J. Clin. Invest. Philip M. Barger, et al. 105:1723 doi:10.1172/JCI9056 [Go to this article.]

Figure 4
Inhibition of the ERK-MAPK pathway blocks the repressive effects of PE on PPARα-mediated control of MCPT.Luc.781. (a) Rat neonatal cardiac myocytes in serum-free media were transfected with MCPT.Luc.781, followed 12 hours later by exposure to PE, PD98059 (PD; 50 μM), or vehicle (DMSO and water). Bars represent mean luciferase activity (RLU) corrected for pSV40–β-Gal activity. ^ASignificantly different from control. (b) Top: Schematic diagram of mouse PPARα showing the location of putative MAPK recognition sites (potential target serines are underlined). Center: Gel autoradiograph containing samples from the in vitro phosphorylation studies performed with activated ERK2 and bacterially expressed, FLAG epitope–tagged, wild-type (WT) PPARα or mutant PPARα proteins containing serine-to-alanine mutations, either at amino acids 6, 12, and 21 (S6-21A), or at amino acids 6, 12, 21, 73, 76, and 77 (S6-77A). Bottom: Western blot analysis of the phosphoprotein samples using anti-FLAG antisera (to control for loading).