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. Author manuscript; available in PMC: 2014 Apr 26.
Published in final edited form as: Circ Res. 2013 Mar 13;112(9):1244–1252. doi: 10.1161/CIRCRESAHA.113.301084

Figure 6. Raf-1 phosphorylation on an autoinhibitory site is increased in the cardiomyocyte transduced with Ad-Pin1.

Figure 6

A, Proximity ligation assay (PLA) showing direct interaction of Pin1 with Raf-1 in cardiomyocytes (green dots, white arrows) with (right) or without stimulation (left). Cardiomyocytes were also stained with tropomyosin (Tmyo, red) and To-pro3 (blue). B, Immunoblots showing time course analysis for Raf-1 phosphorylation on Ser259 (pRaf) after serum stimulation in EGFP and Pin1 treated NRCMs (upper panel). Densitometric quantification is shown in the lower panel for pRaf. n=5. * p<0.05 versus control at the same time point. pRaf protein levels were normalized with GAPDH as a loading control. C, Immunoblots showing time course analysis for pRaf after phenylephrine (PE) stimulation (upper panel). Densitometric quantification is shown in the lower panel for pRaf. n=5. * p<0.05 versus control at the same time point. pRaf protein levels were normalized with GAPDH as a loading control. D, Schematic showing the mechanistic impact of Pin1 depletion as well as over-expression upon cardiac hypertrophy.