Traffic of prion protein between different compartments on the neuronal surface, and the propagation of prion disease.

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 Lett

journal_title

FEBS letters

authors

Morris RJ,Parkyn CJ,Jen A

doi

10.1016/j.febslet.2006.07.053

subject

Has Abstract

pub_date

2006-10-09 00:00:00

pages

5565-71

issue

23

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(06)00894-5

journal_volume

580

pub_type

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