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. 2014 Feb;85(2):357–367. doi: 10.1124/mol.113.090613

Fig. 3.

Fig. 3.

A cell-permeable peptide (Wt-PS) that disrupts interactions between PKARIα and RSK1 activates RSK1 and induces apoptosis in HL-1 cardiomyocytes. (A) Serum-starved HL-1 cells were incubated with 2 μM of the peptide corresponding to the pseudosubstrate region of PKARIα (Wt-PS) or the same peptide-harboring mutations (Mut-PS) either in the presence or absence of SL0101 (50 μM) for 24 hours. Cell lysates were subjected to Western analysis for the various indicated proteins as well as phospho-S732 RSK1 and phospho-PKA substrates. (B) Quantification of data from Western blots of three different experiments normalized for actin (loading control). For phospho-PKA substrate, the 66-kDa band was quantified. Data shown are means ± S.E.M. *P < 0.05. Ctr, control.