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A dystroglycan mutation associated with limb-girdle muscular dystrophy.
TLDR
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.
Immunosuppression and Resultant Viral Persistence by Specific Viral Targeting of Dendritic Cells
TLDR
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.
Viral targeting of hematopoietic progenitors and inhibition of DC maturation as a dual strategy for immune subversion.
TLDR
A virus can evolve a strategy to boost its survival by preventing the maturation of DCs from infected progenitor cells and by reducing the expression of antigen-presenting and costimulatory molecules on developed DCs.
O-Mannosyl Phosphorylation of Alpha-Dystroglycan Is Required for Laminin Binding
TLDR
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.
The Trypanosoma brucei cAMP phosphodiesterases TbrPDEBl and TbrPDEB2: flagellar enzymes that are essential for parasite virulence
TLDR
It is demonstrated that TbrPDEB1 and T brPDEB2 are essential for virulence, making them valuable potential targets for new PDE‐inhibitor based trypanocidal drugs and compatible with the notion that the flagellum of T. brucei is an important site of cAMP signaling.
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