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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 6. Calcineurin inhibition blocks the hypertrophy induced by wild-type and L613V RAF1 proteins.

Figure 6

Neonatal rat cardiomyocytes were infected with Ad.GFP, Ad.RAF1WT and Ad.RAF1L613V and treated with cyclosporine after 48 hours. Seventy-two hours post infection, cardiomyocytes were analyzed for protein synthesis rates (a) and steady-state mRNA levels of Anf (b), Acta1 (c) and Myh7 (d). *P <0.01 vs untreated Ad.GFP. Mean values ± SD of three independent experiments are shown. Raf1 complexes with calcineurin (e) Immunoblots with the indicated antibodies after immunoprecipitation with anti-calcineurin antibody, rabbit pre-immune IgG (rIgG1) or Gapdh as negative control (NC) and reprobed for calcineurin (e) Immunoblots with the indicated antibodies after immunoprecipitation with anti-RAF1 antibody, mouse pre-immune IgG (mIgG1) or Gapdh as negative control (NC) and reprobed for Raf1 (f).