Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein
Identifieur interne : 000346 ( PascalFrancis/Checkpoint ); précédent : 000345; suivant : 000347Identification 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.
Descripteurs français
- Pascal (Inist)
English descriptors
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:
- Canada, République populaire de Chine, États-Unis
- Washington (État)
- Seattle
- Université de Washington
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Beyer</name><affiliation wicri:level="4"><inist: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></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Shengdi Chen" sort="Shengdi Chen" uniqKey="Shengdi Chen" last="Shengdi Chen">SHENGDI CHEN</name><affiliation wicri:level="1"><inist: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></inist:fA14><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><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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0295594</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0295594 INIST</idno><idno type="RBID">Pascal:10-0295594</idno><idno type="wicri:Area/PascalFrancis/Corpus">000429</idno><idno type="wicri:Area/PascalFrancis/Curation">000848</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000346</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000346</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Identification of ciliary neurotrophic factor receptor α as a mediator of neurotoxicity induced by α-synuclein</title><author><name sortKey="Jun Liu" sort="Jun Liu" uniqKey="Jun Liu" last="Jun Liu">JUN LIU</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>République populaire de Chine</country><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist: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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author><author><name sortKey="Min Shi" sort="Min Shi" uniqKey="Min Shi" last="Min Shi">MIN SHI</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author><author><name sortKey="Zhen Hong" sort="Zhen Hong" uniqKey="Zhen Hong" last="Zhen Hong">ZHEN HONG</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>République populaire de Chine</country><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Jianpeng Zhang" sort="Jianpeng Zhang" uniqKey="Jianpeng Zhang" last="Jianpeng Zhang">JIANPENG ZHANG</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author><author><name sortKey="Bradner, Joshua" sort="Bradner, Joshua" uniqKey="Bradner J" first="Joshua" last="Bradner">Joshua Bradner</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author><author><name sortKey="Quinn, Thomas" sort="Quinn, Thomas" uniqKey="Quinn T" first="Thomas" last="Quinn">Thomas Quinn</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author><author><name sortKey="Beyer, Richard P" sort="Beyer, Richard P" uniqKey="Beyer R" first="Richard P." last="Beyer">Richard P. Beyer</name><affiliation wicri:level="4"><inist: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></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation wicri:level="1"><inist: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></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Shengdi Chen" sort="Shengdi Chen" uniqKey="Shengdi Chen" last="Shengdi Chen">SHENGDI CHEN</name><affiliation wicri:level="1"><inist: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></inist:fA14><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><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></inist:fA14><country>États-Unis</country><wicri:noRegion>Seattle, WA</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Proteomics : (Weinheim. Print)</title><title level="j" type="abbreviated">Proteomics : (Weinh., Print)</title><idno type="ISSN">1615-9853</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Proteomics : (Weinheim. Print)</title><title level="j" type="abbreviated">Proteomics : (Weinh., Print)</title><idno type="ISSN">1615-9853</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ciliary neurotrophic factor</term><term>Identification</term><term>Parkinson disease</term><term>Proteomics</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Identification</term><term>Facteur CNTF</term><term>Protéomique</term><term>Maladie de Parkinson</term></keywords></textClass></profileDesc></teiHeader><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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1615-9853</s0></fA01><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></inist><affiliations><list><country><li>Canada</li><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Jun Liu" sort="Jun Liu" uniqKey="Jun Liu" last="Jun Liu">JUN LIU</name></noRegion><name sortKey="Shengdi Chen" sort="Shengdi Chen" uniqKey="Shengdi Chen" last="Shengdi Chen">SHENGDI CHEN</name><name sortKey="Zhen Hong" sort="Zhen Hong" uniqKey="Zhen Hong" last="Zhen Hong">ZHEN HONG</name></country><country name="États-Unis"><noRegion><name sortKey="Jun Liu" sort="Jun Liu" uniqKey="Jun Liu" last="Jun Liu">JUN LIU</name></noRegion><name sortKey="Beyer, Richard P" sort="Beyer, Richard P" uniqKey="Beyer R" first="Richard P." last="Beyer">Richard P. Beyer</name><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><name sortKey="Jing Zhang" sort="Jing Zhang" uniqKey="Jing Zhang" last="Jing Zhang">JING ZHANG</name><name sortKey="Min Shi" sort="Min Shi" uniqKey="Min Shi" last="Min Shi">MIN SHI</name><name sortKey="Quinn, Thomas" sort="Quinn, Thomas" uniqKey="Quinn T" first="Thomas" last="Quinn">Thomas Quinn</name></country><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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