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@ARTICLE{Marbach:150199,
author = {Marbach, Jendrik and Zentis, Peter and Ellinger, Philipp
and Müller, Henrik and Birkmann, Eva},
title = {{E}xpression and characterisation of fully
posttranslationally modified cellular prion protein in
{P}ichia pastoris},
journal = {Biological chemistry},
volume = {394},
number = {11},
issn = {1437-4315},
address = {Berlin [u.a.]},
publisher = {de Gruyter},
reportid = {FZJ-2014-00278},
pages = {1475-1483},
year = {2013},
abstract = {Prion diseases are fatal neurodegenerative diseases which
occur as sporadic, genetic, and transmissible disorders. A
molecular hallmark of prion diseases is the conformational
conversion of the host-encoded cellular form of the prion
protein (PrPC) into its misfolded pathogenic isoform
(PrPSc). PrPSc is the main component of the pathological and
infectious prion agent. The study of the conversion
mechanism from PrPC to PrPSc is a major field in prion
research. PrPC is glycosylated and attached to the plasma
membrane via its glycosyl phosphatidyl inositol
(GPI)-anchor. In this study we established and characterised
the expression of fully posttranslationally modified
mammalian Syrian golden hamster PrPC in the yeast Pichia
pastoris using native PrPC-specific N- and C-terminal signal
sequences. In vivo as well as in vitro-studies demonstrated
that the signal sequences controlled posttranslational
processing and trafficking of native PrPC, resulting in PrPC
localised in the plasma membrane of P. pastoris. In
addition, the glycosylation pattern of native PrPC could be
confirmed.},
cin = {ICS-6},
ddc = {540},
cid = {I:(DE-Juel1)ICS-6-20110106},
pnm = {452 - Structural Biology (POF2-452)},
pid = {G:(DE-HGF)POF2-452},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000325717100011},
doi = {10.1515/hsz-2013-0180},
url = {https://juser.fz-juelich.de/record/150199},
}