Glycosylation deficiency at either one of the two glycan attachment sites of cellular prion protein preserves susceptibility to bovine spongiform encephalopathy and scrapie infections.

Publikationen als Autor:in / Herausgeber:in der Vetmeduni

Saalmüller, Armin

Schlagwörter

Animals; Binding Sites; Biotinylation; Blotting, Western; Brain/pathology; CHO Cells; Cattle; Cell Line; Cell Line, Tumor; Cell Separation; Cloning, Molecular; Cricetinae; Disulfides/chemistry; Encephalopathy, Bovine Spongiform/metabolism*; Flow Cytometry; Glycosylation; Immunoprecipitation; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mutation; Polysaccharides/chemistry*; Prion Diseases/metabolism; Prions/chemistry*; Protein Isoforms; Scrapie/metabolism*; Transgenes;

ISSN/eISSN

0021-9258 -

WoS ID

WOS:000225680600062