Stefan Kunz

TL;DR: It is demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy), commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein.

TL;DR: Findings indicate that receptor–virus interaction on dendritic cells in vivo can be an essential step in the initiation of virus-induced immunosuppression and viral persistence.

TL;DR: It is found that VAMP2 is delivered to the surface of both axons and dendrites, but preferentially endocytosed from the dendritic membrane, showing that neurons use two distinct mechanisms to polarize proteins to the axonal domain: selective retention and selective delivery.

TL;DR: It is shown that both the N-terminal domain and a portion of the mucin-like domain of alpha-dystroglycan are essential for high-affinity laminin-receptor function.

TL;DR: In vitro and in vivo studies showed that the mutation impairs the receptor function of dystroglycan in skeletal muscle and brain by inhibiting the post-translational modification of the phosphorylated O-mannosyl glycans on α-dystrogycan that is required for high-affinity binding to laminin.