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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: J Mol Cell Cardiol. 2011 Apr 8;51(1):4–15. doi: 10.1016/j.yjmcc.2011.03.001

Figure 4. L613V RAF1 but not wild-type RAF1 causes cardiomyocyte hypertrophy via Nfat.

Figure 4

(a) Nfat activity was determined in neonatal rat cardiomyocytes infected with Ad.GFP, Ad.RAF1WT and Ad.RAF1L613V along with Ad.NFAT-LUC. Luciferase activity shown as relative light units (RLU) represent mean values ± SD of three independent experiments. *P <0.001 vs Ad.GFP. Neonatal rat cardiomyocytes were co-infected with Ad.GFP, Ad.RAF1WT and Ad.RAF1L613V along with Ad.VIVIT (treated) that blocks NFAT specifically. Seventy-two hours hours post infection, cardiomyocytes were analyzed for protein synthesis rates (b) and steady-state mRNA levels of Anf (c), Acta1 (d) and Myh7 (e). *p <0.01 vs. untreated Ad.GFP; #p <0.01 vs. treated Ad.GFP. Mean values ± SD of three independent experiments are shown.