Abstract:
:The key mechanism in prion disease is the conversion of cellular prion protein into an altered, pathogenic conformation, in which cellular mechanisms play a poorly understood role. Both forms of prion protein are lipid-anchored and reside in rafts that appear to protect the native conformation against conversion. Neurons rapidly traffic their cellular prion protein out of its lipid rafts to be endocytosed via coated pits before recycling back to the cell surface. It is argued in this review that understanding the mechanism of this trafficking holds the key to understanding the cellular role in the conformational conversion of prion protein.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Morris RJ,Parkyn CJ,Jen Adoi
10.1016/j.febslet.2006.07.053subject
Has Abstractpub_date
2006-10-09 00:00:00pages
5565-71issue
23eissn
0014-5793issn
1873-3468pii
S0014-5793(06)00894-5journal_volume
580pub_type
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