RNA-binding disturbances as a continuum from spinocerebellar ataxia type 2 to Parkinson disease.
Identifieur interne : 000055 ( PubMed/Corpus ); précédent : 000054; suivant : 000056RNA-binding disturbances as a continuum from spinocerebellar ataxia type 2 to Parkinson disease.
Auteurs : Aurore Nkiliza ; Eugénie Mutez ; Clémence Simonin ; Frédéric Leprêtre ; Aurélie Duflot ; Martin Figeac ; Céline Villenet ; Pierre Semaille ; Thomas Comptdaer ; Alexandre Genet ; Bernard Sablonnière ; David Devos ; Luc Defebvre ; Alain Destée ; Marie-Christine Chartier-HarlinSource :
- Neurobiology of disease [ 1095-953X ] ; 2016.
Abstract
CAG triplet expansions in Ataxin-2 gene (ATXN2) cause spinocerebellar ataxia type 2 and have a role that remains to be clarified in Parkinson's disease (PD). To study the molecular events associated with these expansions, we sequenced them and analyzed the transcriptome from blood cells of controls and three patient groups diagnosed with spinocerebellar ataxia type 2 (herein referred to as SCA2c) or PD with or without ATXN2 triplet expansions (named SCA2p). The transcriptome profiles of these 40 patients revealed three main observations: i) a specific pattern of pathways related to cellular contacts, proliferation and differentiation associated with SCA2p group, ii) similarities between the SCA2p and sporadic PD groups in genes and pathways known to be altered in PD such as Wnt, Ephrin and Leukocyte extravasation signaling iii) RNA metabolism disturbances with "RNA-binding" and "poly(A) RNA-binding" as a common feature in all groups. Remarkably, disturbances of ALS signaling were shared between SCA2p and sporadic PD suggesting common molecular dysfunctions in PD and ALS including CACNA1, hnRNP, DDX and PABPC gene family perturbations. Interestingly, the transcriptome profiles of patients with parkinsonian phenotypes were prevalently associated with alterations of translation while SCA2c and PD patients presented perturbations of splicing. While ATXN2 RNA expression was not perturbed, its protein expression in immortalized lymphoblastoid cells was significantly decreased in SCA2c and SCA2p versus control groups assuming post-transcriptional biological perturbations. In conclusion, the transcriptome data do not exclude the role of ATXN2 mutated alleles in PD but its decrease protein expression in both SCA2c and SCA2p patients suggest a potential involvement of this gene in PD. The perturbations of "RNA-binding" and "poly(A) RNA-binding" molecular functions in the three patient groups as well as gene deregulations of factors not yet described in PD but known to be deleterious in other neurological conditions, suggest the existence of RNA-binding disturbances as a continuum between spinocerebellar ataxia type 2 and Parkinson's disease.
DOI: 10.1016/j.nbd.2016.09.014
PubMed: 27663142
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Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Simonin, Clemence" sort="Simonin, Clemence" uniqKey="Simonin C" first="Clémence" last="Simonin">Clémence Simonin</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lepretre, Frederic" sort="Lepretre, Frederic" uniqKey="Lepretre F" first="Frédéric" last="Leprêtre">Frédéric Leprêtre</name><affiliation><nlm:affiliation>Univ. 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Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Comptdaer, Thomas" sort="Comptdaer, Thomas" uniqKey="Comptdaer T" first="Thomas" last="Comptdaer">Thomas Comptdaer</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Genet, Alexandre" sort="Genet, Alexandre" uniqKey="Genet A" first="Alexandre" last="Genet">Alexandre Genet</name><affiliation><nlm:affiliation>CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Sablonniere, Bernard" sort="Sablonniere, Bernard" uniqKey="Sablonniere B" first="Bernard" last="Sablonnière">Bernard Sablonnière</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name><affiliation><nlm:affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Defebvre, Luc" sort="Defebvre, Luc" uniqKey="Defebvre L" first="Luc" last="Defebvre">Luc Defebvre</name><affiliation><nlm:affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Destee, Alain" sort="Destee, Alain" uniqKey="Destee A" first="Alain" last="Destée">Alain Destée</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Chartier Harlin, Marie Christine" sort="Chartier Harlin, Marie Christine" uniqKey="Chartier Harlin M" first="Marie-Christine" last="Chartier-Harlin">Marie-Christine Chartier-Harlin</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France. Electronic address: marie-christine.chartier-harlin@inserm.fr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27663142</idno><idno type="pmid">27663142</idno><idno type="doi">10.1016/j.nbd.2016.09.014</idno><idno type="wicri:Area/PubMed/Corpus">000055</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000055</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">RNA-binding disturbances as a continuum from spinocerebellar ataxia type 2 to Parkinson disease.</title><author><name sortKey="Nkiliza, Aurore" sort="Nkiliza, Aurore" uniqKey="Nkiliza A" first="Aurore" last="Nkiliza">Aurore Nkiliza</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mutez, Eugenie" sort="Mutez, Eugenie" uniqKey="Mutez E" first="Eugénie" last="Mutez">Eugénie Mutez</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Simonin, Clemence" sort="Simonin, Clemence" uniqKey="Simonin C" first="Clémence" last="Simonin">Clémence Simonin</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lepretre, Frederic" sort="Lepretre, Frederic" uniqKey="Lepretre F" first="Frédéric" last="Leprêtre">Frédéric Leprêtre</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Duflot, Aurelie" sort="Duflot, Aurelie" uniqKey="Duflot A" first="Aurélie" last="Duflot">Aurélie Duflot</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Figeac, Martin" sort="Figeac, Martin" uniqKey="Figeac M" first="Martin" last="Figeac">Martin Figeac</name><affiliation><nlm:affiliation>Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Villenet, Celine" sort="Villenet, Celine" uniqKey="Villenet C" first="Céline" last="Villenet">Céline Villenet</name><affiliation><nlm:affiliation>Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Semaille, Pierre" sort="Semaille, Pierre" uniqKey="Semaille P" first="Pierre" last="Semaille">Pierre Semaille</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Comptdaer, Thomas" sort="Comptdaer, Thomas" uniqKey="Comptdaer T" first="Thomas" last="Comptdaer">Thomas Comptdaer</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Genet, Alexandre" sort="Genet, Alexandre" uniqKey="Genet A" first="Alexandre" last="Genet">Alexandre Genet</name><affiliation><nlm:affiliation>CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Sablonniere, Bernard" sort="Sablonniere, Bernard" uniqKey="Sablonniere B" first="Bernard" last="Sablonnière">Bernard Sablonnière</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Devos, David" sort="Devos, David" uniqKey="Devos D" first="David" last="Devos">David Devos</name><affiliation><nlm:affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Defebvre, Luc" sort="Defebvre, Luc" uniqKey="Defebvre L" first="Luc" last="Defebvre">Luc Defebvre</name><affiliation><nlm:affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Destee, Alain" sort="Destee, Alain" uniqKey="Destee A" first="Alain" last="Destée">Alain Destée</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</nlm:affiliation></affiliation></author><author><name sortKey="Chartier Harlin, Marie Christine" sort="Chartier Harlin, Marie Christine" uniqKey="Chartier Harlin M" first="Marie-Christine" last="Chartier-Harlin">Marie-Christine Chartier-Harlin</name><affiliation><nlm:affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France. Electronic address: marie-christine.chartier-harlin@inserm.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CAG triplet expansions in Ataxin-2 gene (ATXN2) cause spinocerebellar ataxia type 2 and have a role that remains to be clarified in Parkinson's disease (PD). To study the molecular events associated with these expansions, we sequenced them and analyzed the transcriptome from blood cells of controls and three patient groups diagnosed with spinocerebellar ataxia type 2 (herein referred to as SCA2c) or PD with or without ATXN2 triplet expansions (named SCA2p). The transcriptome profiles of these 40 patients revealed three main observations: i) a specific pattern of pathways related to cellular contacts, proliferation and differentiation associated with SCA2p group, ii) similarities between the SCA2p and sporadic PD groups in genes and pathways known to be altered in PD such as Wnt, Ephrin and Leukocyte extravasation signaling iii) RNA metabolism disturbances with "RNA-binding" and "poly(A) RNA-binding" as a common feature in all groups. Remarkably, disturbances of ALS signaling were shared between SCA2p and sporadic PD suggesting common molecular dysfunctions in PD and ALS including CACNA1, hnRNP, DDX and PABPC gene family perturbations. Interestingly, the transcriptome profiles of patients with parkinsonian phenotypes were prevalently associated with alterations of translation while SCA2c and PD patients presented perturbations of splicing. While ATXN2 RNA expression was not perturbed, its protein expression in immortalized lymphoblastoid cells was significantly decreased in SCA2c and SCA2p versus control groups assuming post-transcriptional biological perturbations. In conclusion, the transcriptome data do not exclude the role of ATXN2 mutated alleles in PD but its decrease protein expression in both SCA2c and SCA2p patients suggest a potential involvement of this gene in PD. The perturbations of "RNA-binding" and "poly(A) RNA-binding" molecular functions in the three patient groups as well as gene deregulations of factors not yet described in PD but known to be deleterious in other neurological conditions, suggest the existence of RNA-binding disturbances as a continuum between spinocerebellar ataxia type 2 and Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27663142</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>24</Day></DateCreated><DateRevised><Year>2016</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>96</Volume><PubDate><Year>2016</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>RNA-binding disturbances as a continuum from spinocerebellar ataxia type 2 to Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>312-322</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(16)30230-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2016.09.014</ELocationID><Abstract><AbstractText NlmCategory="UNASSIGNED">CAG triplet expansions in Ataxin-2 gene (ATXN2) cause spinocerebellar ataxia type 2 and have a role that remains to be clarified in Parkinson's disease (PD). To study the molecular events associated with these expansions, we sequenced them and analyzed the transcriptome from blood cells of controls and three patient groups diagnosed with spinocerebellar ataxia type 2 (herein referred to as SCA2c) or PD with or without ATXN2 triplet expansions (named SCA2p). The transcriptome profiles of these 40 patients revealed three main observations: i) a specific pattern of pathways related to cellular contacts, proliferation and differentiation associated with SCA2p group, ii) similarities between the SCA2p and sporadic PD groups in genes and pathways known to be altered in PD such as Wnt, Ephrin and Leukocyte extravasation signaling iii) RNA metabolism disturbances with "RNA-binding" and "poly(A) RNA-binding" as a common feature in all groups. Remarkably, disturbances of ALS signaling were shared between SCA2p and sporadic PD suggesting common molecular dysfunctions in PD and ALS including CACNA1, hnRNP, DDX and PABPC gene family perturbations. Interestingly, the transcriptome profiles of patients with parkinsonian phenotypes were prevalently associated with alterations of translation while SCA2c and PD patients presented perturbations of splicing. While ATXN2 RNA expression was not perturbed, its protein expression in immortalized lymphoblastoid cells was significantly decreased in SCA2c and SCA2p versus control groups assuming post-transcriptional biological perturbations. In conclusion, the transcriptome data do not exclude the role of ATXN2 mutated alleles in PD but its decrease protein expression in both SCA2c and SCA2p patients suggest a potential involvement of this gene in PD. The perturbations of "RNA-binding" and "poly(A) RNA-binding" molecular functions in the three patient groups as well as gene deregulations of factors not yet described in PD but known to be deleterious in other neurological conditions, suggest the existence of RNA-binding disturbances as a continuum between spinocerebellar ataxia type 2 and Parkinson's disease.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nkiliza</LastName><ForeName>Aurore</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mutez</LastName><ForeName>Eugénie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simonin</LastName><ForeName>Clémence</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leprêtre</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duflot</LastName><ForeName>Aurélie</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Figeac</LastName><ForeName>Martin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Villenet</LastName><ForeName>Céline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Univ. Lille, CHU Lille, IRCL, Structural and Functional Genomics Core Facility, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Semaille</LastName><ForeName>Pierre</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Comptdaer</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Genet</LastName><ForeName>Alexandre</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sablonnière</LastName><ForeName>Bernard</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; CHU Lille, Centre de Biologie Pathologie, Unité de Neurobiologie, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Devos</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Defebvre</LastName><ForeName>Luc</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Destée</LastName><ForeName>Alain</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France; CHU Lille, Neurologie et Pathologie du Mouvement, F-59000 Lille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chartier-Harlin</LastName><ForeName>Marie-Christine</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Univ. Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, F-59000 Lille, France; Inserm, UMR-S 1172, Team "Early stages of Parkinson's disease", F-59000 Lille, France. Electronic address: marie-christine.chartier-harlin@inserm.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>09</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ATXN2 CAG expansions</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">RNA metabolism</Keyword><Keyword MajorTopicYN="N">Spinocerebellar ataxia type 2</Keyword><Keyword MajorTopicYN="N">Translation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>05</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>09</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>10</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27663142</ArticleId><ArticleId IdType="pii">S0969-9961(16)30230-3</ArticleId><ArticleId IdType="doi">10.1016/j.nbd.2016.09.014</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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