Cells control the adhesion protein desmoplakin by modifying the tail end of the protein, and this process goes awry in some patients with arrhythmogenic cardiomyopathy, according to a study in The Journal of Cell Biology.
Desmoplakin (green) normally resides at cell-to-cell junctions (left), but in cells that can’t modify it (right), it associates with intermediate filaments (red).
Credit: Albrecht et al., 2015
GSK3- and PRMT-1–dependent modifications of desmoplakin control desmoplakin–cytoskeleton dynamics. Albrecht, L.V., et al. 2015. J. Cell Biol. doi:10.1083/jcb.201406020