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@ARTICLE{Poojari:140001,
author = {Poojari, Chetan and Xiao, D. and Batista, V. S. and
Strodel, Birgit},
title = {{M}embrane {P}ermeation {I}nduced by {A}ggregates of
{H}uman {I}slet {A}myloid {P}olypeptides},
journal = {Biophysical journal},
volume = {105},
issn = {0006-3495},
address = {New York, NY},
publisher = {Rockefeller Univ. Press},
reportid = {FZJ-2013-05968},
pages = {2323-2332},
year = {2013},
abstract = {Several neurodegenerative diseases such as Alzheimer’s
and Parkinson’s diseases as well as nonneuropathic
diseases such as type II diabetes and atrial amyloidosis are
associated with aggregation of amyloid polypeptides into
fibrillar structures, or plaques. In this study, we use
molecular dynamics simulations to test the stability and
orientation of membrane-embedded aggregates of the human
islet amyloid polypeptide (hIAPP) implicated in type II
diabetes. We find that in both monolayers and bilayers of
dipalmitoylphosphatidylglycerol (DPPG) hIAPP trimers and
tetramers remain inside the membranes and preserve their
β-sheet secondary structure. Lipid bilayer-inserted hIAPP
trimers and tetramers orient inside DPPG at 60° relative to
the membrane/water interface and lead to water permeation
and Na+ intrusion, consistent with ion-toxicity in islet
β-cells. In particular, hIAPP trimers form a water-filled
β-sandwich that induce water permeability comparable with
channel-forming proteins, such as aquaporins and
gramicidin-A. The predicted disruptive orientation is
consistent with the amphiphilic properties of the hIAPP
aggregates and could be probed by chiral sum frequency
generation (SFG) spectroscopy, as predicted by the simulated
SFG spectra.},
cin = {ICS-6},
ddc = {570},
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:000327285100013},
pubmed = {pmid:24268144},
doi = {10.1016/j.bpj.2013.09.045},
url = {https://juser.fz-juelich.de/record/140001},
}