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dc.contributor.author
Yu, Chengli
dc.contributor.author
Gao, Jing
dc.contributor.author
Zhou, Yanting
dc.contributor.author
Chen, Xiangling
dc.contributor.author
Xiao, Ruoxuan
dc.contributor.author
Zheng, Jing
dc.contributor.author
Liu, Yansheng
dc.contributor.author
Zhou, Hu
dc.date.accessioned
2019-08-20T12:37:58Z
dc.date.available
2017-06-12T18:09:19Z
dc.date.available
2019-08-20T12:37:58Z
dc.date.issued
2016-12
dc.identifier.issn
1664-042X
dc.identifier.other
10.3389/fphys.2016.00635
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/125520
dc.identifier.doi
10.3929/ethz-b-000125520
dc.description.abstract
Alzheimer's disease (AD) is a progressive and irreversible neurological disorder that impairs the living quality of old population and even life spans. New compounds have shown potential inneuroprotective effects in AD, such as GFKP-19, a 2-pyrrolidone derivative which has been proved to enhance the memory of dysmnesia mouse. The molecular mechanisms remain to be established for these drug candidates. Large-scale phosphoproteomic approach has been evolved rapidly in the last several years, which holds the potential to provide a useful toolkit to understand cellular signaling underlying drug effects. To establish and test such a method, we accurately analyzed the deep quantitative phosphoproteome of the neuro-2a cells treated with and without GFKP-19 using triple SILAC labeling. A total of 14,761 Class I phosphosites were quantified between controls, damaged, and protected conditions using the high resolution mass spectrometry, with a decent inter-mass spectrometer reproducibility for even subtle regulatory events. Our data suggests that GFKP-19 can reverse Aβ25−35 induced phosphorylation change in neuro-2a cells, and might protect the neuron system in two ways: firstly, it may decrease oxidative damage and inflammation induced by NO via down regulating the phosphorylation of nitric oxide synthase NOS1 at S847; Secondly, it may decrease tau protein phosphorylation through down-regulating the phosphorylation level of MAPK14 at T180. All mass spectrometry data are available via ProteomeXchange with identifier PXD005312.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Frontiers Research Foundation
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
phosphoproteomics
en_US
dc.subject
Alzheimer’s disease
en_US
dc.subject
drug effect
en_US
dc.subject
mass spectrometry
en_US
dc.subject
neutronal cells
en_US
dc.title
Deep Phosphoproteomic Measurements Pinpointing Drug Induced Protective Mechanisms in Neuronal Cells
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2016-12-23
ethz.journal.title
Frontiers in Physiology
ethz.journal.volume
7
en_US
ethz.journal.abbreviated
Front Physiol
ethz.pages.start
635
en_US
ethz.size
14 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.identifier.nebis
006386708
ethz.publication.place
Lausanne
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2017-06-12T18:10:03Z
ethz.source
ECIT
ethz.identifier.importid
imp5936551191f1e58790
ethz.ecitpid
pub:188128
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-14T14:08:32Z
ethz.rosetta.lastUpdated
2019-08-20T12:38:15Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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