ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000429

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

Identifieur interne : 000429 ( PascalFrancis/Corpus ); précédent : 000428; suivant : 000430

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

Auteurs : JUN LIU ; MIN SHI ; ZHEN HONG ; JIANPENG ZHANG ; Joshua Bradner ; Thomas Quinn ; Richard P. Beyer ; Patrick L. Mcgeer ; SHENGDI CHEN ; JING ZHANG

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 JUN LIU`
A11	`02`	`1`		`@1 MIN SHI`
A11	`03`	`1`		`@1 ZHEN HONG`
A11	`04`	`1`		`@1 JIANPENG ZHANG`
A11	`05`	`1`		`@1 BRADNER (Joshua)`
A11	`06`	`1`		`@1 QUINN (Thomas)`
A11	`07`	`1`		`@1 BEYER (Richard P.)`
A11	`08`	`1`		`@1 MCGEER (Patrick L.)`
A11	`09`	`1`		`@1 SHENGDI CHEN`
A11	`10`	`1`		`@1 JING ZHANG`
A14	`01`			`@1 Department of Neurology and Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine @2 Shanghai @3 CHN @Z 1 aut. @Z 3 aut. @Z 9 aut.`
A14	`02`			`@1 Department of Pathology, University of Washington School of Medicine @2 Seattle, WA @3 USA @Z 1 aut. @Z 2 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 10 aut.`
A14	`03`			`@1 Department of Environmental and Occupational Health Sciences, University of Washington @2 Seattle, WA @3 USA @Z 7 aut.`
A14	`04`			`@1 Kinsmen Laboratory of Neurological Research, University of British Columbia @2 Vancouver, BC @3 CAN @Z 8 aut.`
A20				`@1 2138-2150`
A21				`@1 2010`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 27206 @5 354000170413940060`
A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 43 ref.`
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C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002A02D10`
C02	`02`	`X`		`@0 002B17G`
C02	`03`	`X`		`@0 002B17A01`
C03	`01`	`X`	`FRE`	`@0 Identification @5 05`
C03	`01`	`X`	`ENG`	`@0 Identification @5 05`
C03	`01`	`X`	`SPA`	`@0 Identificación @5 05`
C03	`02`	`X`	`FRE`	`@0 Facteur CNTF @5 06`
C03	`02`	`X`	`ENG`	`@0 Ciliary neurotrophic factor @5 06`
C03	`02`	`X`	`SPA`	`@0 Factor neurotrófico ciliar @5 06`
C03	`03`	`X`	`FRE`	`@0 Protéomique @5 07`
C03	`03`	`X`	`ENG`	`@0 Proteomics @5 07`
C03	`03`	`X`	`SPA`	`@0 Proteómica @5 07`
C03	`04`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 14`
C03	`04`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 14`
C03	`04`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 14`
C07	`01`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 13`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 13`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 13`
C07	`02`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 16`
C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 16`
C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 16`
C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 17`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 17`
C07	`03`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 17`
C07	`04`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 18`
C07	`04`	`X`	`ENG`	`@0 Central nervous system disease @5 18`
C07	`04`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 18`
C07	`05`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 19`
C07	`05`	`X`	`ENG`	`@0 Nervous system diseases @5 19`
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Format Inist (serveur)

NO :	PASCAL 10-0295594 INIST
ET :	Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein
AU :	JUN LIU; MIN SHI; ZHEN HONG; JIANPENG ZHANG; BRADNER (Joshua); QUINN (Thomas); BEYER (Richard P.); MCGEER (Patrick L.); SHENGDI CHEN; JING ZHANG
AF :	Department of Neurology and Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine/Shanghai/Chine (1 aut., 3 aut., 9 aut.); Department of Pathology, University of Washington School of Medicine/Seattle, WA/Etats-Unis (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 10 aut.); Department of Environmental and Occupational Health Sciences, University of Washington/Seattle, WA/Etats-Unis (7 aut.); Kinsmen Laboratory of Neurological Research, University of British Columbia/Vancouver, BC/Canada (8 aut.)
DT :	Publication en série; Niveau analytique
SO :	Proteomics : (Weinheim. Print); ISSN 1615-9853; Allemagne; Da. 2010; Vol. 10; No. 11; Pp. 2138-2150; Bibl. 43 ref.
LA :	Anglais
EA :	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.
CC :	002A02D10; 002B17G; 002B17A01
FD :	Identification; Facteur CNTF; Protéomique; Maladie de Parkinson
FG :	Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux
ED :	Identification; Ciliary neurotrophic factor; Proteomics; Parkinson disease
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases
SD :	Identificación; Factor neurotrófico ciliar; Proteómica; Parkinson enfermedad
LO :	INIST-27206.354000170413940060
ID :	10-0295594

Links to Exploration step

Pascal:10-0295594

Le document en format XML

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<author><name sortKey="Jing Zhang" sort="Jing Zhang" uniqKey="Jing Zhang" last="Jing Zhang">JING ZHANG</name>
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<series><title level="j" type="main">Proteomics : (Weinheim. Print)</title>
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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>
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<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1615-9853</s0>
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<fA03 i2="1"><s0>Proteomics : (Weinh., Print)</s0>
</fA03>
<fA05><s2>10</s2>
</fA05>
<fA06><s2>11</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>JUN LIU</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>MIN SHI</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>ZHEN HONG</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>JIANPENG ZHANG</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BRADNER (Joshua)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>QUINN (Thomas)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>BEYER (Richard P.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>MCGEER (Patrick L.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>SHENGDI CHEN</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>JING ZHANG</s1>
</fA11>
<fA14 i1="01"><s1>Department of Neurology and Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Pathology, University of Washington School of Medicine</s1>
<s2>Seattle, WA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Environmental and Occupational Health Sciences, University of Washington</s1>
<s2>Seattle, WA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Kinsmen Laboratory of Neurological Research, University of British Columbia</s1>
<s2>Vancouver, BC</s2>
<s3>CAN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA20><s1>2138-2150</s1>
</fA20>
<fA21><s1>2010</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>27206</s2>
<s5>354000170413940060</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>43 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>10-0295594</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Proteomics : (Weinheim. Print)</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A02D10</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B17A01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Identification</s0>
<s5>05</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Identification</s0>
<s5>05</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Identificación</s0>
<s5>05</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Facteur CNTF</s0>
<s5>06</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Ciliary neurotrophic factor</s0>
<s5>06</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Factor neurotrófico ciliar</s0>
<s5>06</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Protéomique</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Proteomics</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Proteómica</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>13</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>13</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>13</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>16</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>16</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>16</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>17</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>17</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>17</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>18</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>18</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>18</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>19</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>19</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>19</s5>
</fC07>
<fN21><s1>186</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 10-0295594 INIST</NO>
<ET>Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein</ET>
<AU>JUN LIU; MIN SHI; ZHEN HONG; JIANPENG ZHANG; BRADNER (Joshua); QUINN (Thomas); BEYER (Richard P.); MCGEER (Patrick L.); SHENGDI CHEN; JING ZHANG</AU>
<AF>Department of Neurology and Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiaotong University School of Medicine/Shanghai/Chine (1 aut., 3 aut., 9 aut.); Department of Pathology, University of Washington School of Medicine/Seattle, WA/Etats-Unis (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 10 aut.); Department of Environmental and Occupational Health Sciences, University of Washington/Seattle, WA/Etats-Unis (7 aut.); Kinsmen Laboratory of Neurological Research, University of British Columbia/Vancouver, BC/Canada (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Proteomics : (Weinheim. Print); ISSN 1615-9853; Allemagne; Da. 2010; Vol. 10; No. 11; Pp. 2138-2150; Bibl. 43 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002A02D10; 002B17G; 002B17A01</CC>
<FD>Identification; Facteur CNTF; Protéomique; Maladie de Parkinson</FD>
<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central; Pathologie du   système nerveux</FG>
<ED>Identification; Ciliary neurotrophic factor; Proteomics; Parkinson disease</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases</EG>
<SD>Identificación; Factor neurotrófico ciliar; Proteómica; Parkinson enfermedad</SD>
<LO>INIST-27206.354000170413940060</LO>
<ID>10-0295594</ID>
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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

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