A point mutation in GPI-attachment signal peptide accelerates the development of prion disease
A point mutation in GPI-attachment signal peptide accelerates the development of prion disease
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Publisher
Berlin/Heidelberg: Springer Berlin Heidelberg
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Language
English
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Publisher
Berlin/Heidelberg: Springer Berlin Heidelberg
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Scope and Contents
Contents
A missense variant from methionine to arginine at codon 232 (M232R) of the prion protein gene accounts for ~ 15% of Japanese patients with genetic prion diseases. However, pathogenic roles of the M232R substitution for the induction of prion disease have remained elusive because family history is usually absent in patients with M232R. In addition,...
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Full title
A point mutation in GPI-attachment signal peptide accelerates the development of prion disease
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TN_cdi_proquest_miscellaneous_2784383840
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_miscellaneous_2784383840
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ISSN
0001-6322
E-ISSN
1432-0533
DOI
10.1007/s00401-023-02553-5
