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@ARTICLE{Bachmann:134961,
author = {Bachmann, Michael and Strodel, Birgit and Osborne, Kenneth
L.},
title = {{T}hermodynamic analysis of structural transitions during
{GNNQQNY} aggregation},
journal = {Proteins},
volume = {81},
number = {7},
issn = {0887-3585},
address = {New York, NY},
publisher = {Wiley-Liss},
reportid = {FZJ-2013-02976},
pages = {1141 - 1155},
year = {2013},
abstract = {Amyloid protein aggregation characterizes many
neurodegenerative disorders, including Alzheimer's,
Parkinson's, and Creutzfeldt-Jakob disease. Evidence
suggests that amyloid aggregates may share similar
aggregation pathways, implying simulation of full-length
amyloid proteins is not necessary for understanding amyloid
formation. In this study, we simulate GNNQQNY, the
N-terminal prion-determining domain of the yeast protein
Sup35 to investigate the thermodynamics of structural
transitions during aggregation. Utilizing a coarse-grained
model permits equilibration on relevant time scales.
Replica-exchange molecular dynamics is used to gather
simulation statistics at multiple temperatures and clear
energy traps that would aversely impact results.
Investigating the association of 3-, 6-, and 12-chain
GNNQQNY systems by calculating thermodynamic quantities and
orientational order parameters, we determine the aggregation
pathway by studying aggregation states of GNNQQNY. We find
that the aggregation of the hydrophilic GNNQQNY sequence is
mainly driven by H-bond formation, leading to the formation
of β-sheets from the very beginning of the assembly
process. Condensation (aggregation) and ordering take place
simultaneously, which is underpinned by the occurrence of a
single heat capacity peak.},
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:000320474100005},
pubmed = {pmid:23408546},
doi = {10.1002/prot.24263},
url = {https://juser.fz-juelich.de/record/134961},
}