α - Neurexin multiplexes 1 Dystroglycan Binding to α −

نویسندگان

  • Johanna Stahn
  • Dorothee Breuer
  • Martin Klose
  • Gottfried Pohlentz
  • Michael Mormann
  • Markus Missler
چکیده

Carsten Reissner, Johanna Stahn, Dorothee Breuer, Martin Klose, Gottfried Pohlentz, Michael Mormann, and Markus Missler From the Institute of Anatomy and Molecular Neurobiology, Westfälische Wilhelms-University, Vesaliusweg 2-4, 48149 Münster, Germany; Institute of Medical Physics and Biophysics, Westfälische Wilhelms-University Robert-Koch Strasse 31, 48149 Münster, Germany Cluster of Excellence EXC 1003, Cells in Motion, CiM, Münster, Germany;

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Dystroglycan Binding to α-Neurexin Competes with Neurexophilin-1 and Neuroligin in the Brain*

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LARGE Expression Augments the Glycosylation of Glycoproteins in Addition to α-Dystroglycan Conferring Laminin Binding

Mutations in genes encoding glycosyltransferases (and presumed glycosyltransferases) that affect glycosylation and extracellular matrix binding activity of α-dystroglycan (α-DG) cause congenital muscular dystrophies (CMDs) with central nervous system manifestations. Among the identified genes, LARGE is of particular interest because its overexpression rescues glycosylation defects of α-DG in mu...

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Differential glycosylation of α-dystroglycan and proteins other than α-dystroglycan by like-glycosyltransferase.

Genetic defects in like-glycosyltransferase (LARGE) cause congenital muscular dystrophy with central nervous system manifestations. The underlying molecular pathomechanism is the hypoglycosylation of α-dystroglycan (α-DG), which is evidenced by diminished immunoreactivity to IIH6C4 and VIA4-1, antibodies that recognize carbohydrate epitopes. Previous studies indicate that LARGE participates in ...

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تاریخ انتشار 2014