Figure 2.

Cardiac myocytes from the carrier of the p.P961L mutation showed a disrupted sarcomeric distribution of myopalladin and α-actinin. Endomyocardial biopsies obtained from three DCM patients expressing either wild-type or mutant myopalladin (p.R955W and p.P961L) were immunohistochemically stained with either a polyclonal antibody directed against myopalladin or a monoclonal α-actinin antibody. Specific immunoreactivity was detected by incubating the samples with Cy3-labeled secondary antibodies, while nuclei were stained with Hoechst dye.