ParkinsonCanadaV1, Main, Exploration, bibRecord, 001D07

Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein

Identifieur interne : 001D07 ( Main/Exploration ); précédent : 001D06; suivant : 001D08

Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein

Auteurs : JUN LIU [République populaire de Chine, États-Unis] ; MIN SHI [États-Unis] ; ZHEN HONG [République populaire de Chine] ; JIANPENG ZHANG [États-Unis] ; Joshua Bradner [États-Unis] ; Thomas Quinn [États-Unis] ; Richard P. Beyer [États-Unis] ; Patrick L. Mcgeer [Canada] ; SHENGDI CHEN [République populaire de Chine] ; JING ZHANG [États-Unis]

Source :

Proteomics : (Weinheim. Print) [ 1615-9853 ] ; 2010.

RBID : Pascal:10-0295594

Descripteurs français

Pascal (Inist)
- Identification, Facteur CNTF, Protéomique, Maladie de Parkinson.

English descriptors

KwdEn :
- Ciliary neurotrophic factor, Identification, Parkinson disease, Proteomics.

Abstract

Accumulating evidence suggests that extracellular α-synuclein (eSNCA) plays an important role in the pathogenesis of Parkinson's disease or related synucleinopathies by inducing neurotoxicity directly or indirectly via microglial or astroglial activation. However, the mechanisms by which this occurs remain to be characterized. To explore these mechanisms, we combined three biochemical techniques - stable isotope labeling of amino acid in cell cultures (SILAC), biotin labeling of plasma membrane proteins followed by affinity purification, and analysis of unique proteins binding to SNCA peptides on membrane arrays. The SILAC proteomic analysis identified 457 proteins, of which, 245 or 172 proteins belonged to membrane or membrane associated proteins, depending on the various bioinformatics tools used for interpretation. In dopamine neuronal cells treated with eSNCA, the levels of 86 membrane proteins were increased and 35 were decreased compared with untreated cells. In peptide array analysis, 127 proteins were identified as possibly interacting with eSNCA. Of those, seven proteins were overlapped with the membrane proteins that displayed alterations in relative abundance after eSNCA treatment. One was ciliary neurotrophic factor receptor, which appeared to modulate eSNCA-mediated neurotoxicity via mechanisms related to JAK1/ STAT3 signaling but independent of eSNCA endocytosis.

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<country>République populaire de Chine</country>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Jing Zhang" sort="Jing Zhang" uniqKey="Jing Zhang" last="Jing Zhang">JING ZHANG</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Pathology, University of Washington School of Medicine</s1>
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<front><div type="abstract" xml:lang="en">Accumulating evidence suggests that extracellular α-synuclein (eSNCA) plays an important role in the pathogenesis of Parkinson's disease or related synucleinopathies by inducing neurotoxicity directly or indirectly via microglial or astroglial activation. However, the mechanisms by which this occurs remain to be characterized. To explore these mechanisms, we combined three biochemical techniques - stable isotope labeling of amino acid in cell cultures (SILAC), biotin labeling of plasma membrane proteins followed by affinity purification, and analysis of unique proteins binding to SNCA peptides on membrane arrays. The SILAC proteomic analysis identified 457 proteins, of which, 245 or 172 proteins belonged to membrane or membrane associated proteins, depending on the various bioinformatics tools used for interpretation. In dopamine neuronal cells treated with eSNCA, the levels of 86 membrane proteins were increased and 35 were decreased compared with untreated cells. In peptide array analysis, 127 proteins were identified as possibly interacting with eSNCA. Of those, seven proteins were overlapped with the membrane proteins that displayed alterations in relative abundance after eSNCA treatment. One was ciliary neurotrophic factor receptor, which appeared to modulate eSNCA-mediated neurotoxicity via mechanisms related to JAK1/ STAT3 signaling but independent of eSNCA endocytosis.</div>
</front>
</TEI>
<affiliations><list><country><li>Canada</li>
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<li>États-Unis</li>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Jun Liu" sort="Jun Liu" uniqKey="Jun Liu" last="Jun Liu">JUN LIU</name>
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<name sortKey="Bradner, Joshua" sort="Bradner, Joshua" uniqKey="Bradner J" first="Joshua" last="Bradner">Joshua Bradner</name>
<name sortKey="Jianpeng Zhang" sort="Jianpeng Zhang" uniqKey="Jianpeng Zhang" last="Jianpeng Zhang">JIANPENG ZHANG</name>
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<name sortKey="Min Shi" sort="Min Shi" uniqKey="Min Shi" last="Min Shi">MIN SHI</name>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein

Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri