CAMK2B and myotonic dystrophy type 1: Analysis of a mouse model for myotonic dystrophy type 1 specifically lacking the muscle-specific splice variant of CaMK2β (CaMK2βM), which exhibits synapse fragmentation that is rescued by overexpression of CaMK2β12–14 revealed a global increase of MuSK protein expression but ruled out defective MuSK activation as cause of synapse fragmentation.