The TSEs (transmissible spongiform encephalopathies) are not only devastating neurological diseases but also provide a biochemical conundrum; how can a disease agent replicate in the apparent absence of genetic material? The prion hypothesis proposes that the TSE agent is a misfolded form of the host glycoprotein PrP (prion protein). However, a number of questions regarding the hypothesis remain to be addressed. We are using gene-targeted PrP transgenics models to investigate these issues. Here we discuss our recent results that examine the importance of PrP's N-glycans to the misfolding of the protein.
Conference Article| October 26 2005
Glycosylation and misfolding of PrP
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F. Wiseman, E. Cancellotti, J. Manson; Glycosylation and misfolding of PrP. Biochem Soc Trans 26 October 2005; 33 (5): 1094–1095. doi: https://doi.org/10.1042/BST0331094
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