Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.
Identifieur interne : 000664 ( PubMed/Corpus ); précédent : 000663; suivant : 000665Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.
Auteurs : Margot Fournier ; Amandine Roux ; Jérôme Garrigue ; Marie-Paule Muriel ; Paul Blanche ; Hilal A. Lashuel ; John P. Anderson ; Robin Barbour ; Jiping Huang ; Sophie Tezenas Du Montcel ; Alexis Brice ; Olga CortiSource :
- BMC neuroscience [ 1471-2202 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Blotting, Western, Brain (metabolism), Brain (pathology), Disease Models, Animal, Fluorescent Antibody Technique, Humans, Mass Spectrometry, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Microscopy, Electron, Transmission, Motor Skills, Nerve Degeneration (genetics), Nerve Degeneration (pathology), Parkinson Disease (genetics), Parkinson Disease (pathology), Ubiquitin-Protein Ligases (genetics), alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : Ubiquitin-Protein Ligases, alpha-Synuclein.
- genetics : Nerve Degeneration, Parkinson Disease.
- metabolism : Brain.
- pathology : Brain, Nerve Degeneration, Parkinson Disease.
- Animals, Blotting, Western, Disease Models, Animal, Fluorescent Antibody Technique, Humans, Mass Spectrometry, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Microscopy, Electron, Transmission, Motor Skills.
Abstract
Mutations of the gene encoding the major component of Lewy bodies (LB), α-synuclein (α-syn), cause autosomal dominant forms of Parkinson's disease (PD), whereas loss-of-function mutations of the gene encoding the multifunctional E3 ubiquitin-protein ligase Parkin account for autosomal recessive forms of the disease. Parkin overproduction protects against α-syn-dependent neurodegeneration in various in vitro and in vivo models, but it remains unclear whether this process is affected by Parkin deficiency. We addressed this issue, by carrying out more detailed analyses of transgenic mice overproducing the A30P variant of human α-syn (hA30Pα-syn) and with two, one or no parkin knockout alleles.
DOI: 10.1186/1471-2202-14-135
PubMed: 24192137
Links to Exploration step
pubmed:24192137Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.</title><author><name sortKey="Fournier, Margot" sort="Fournier, Margot" uniqKey="Fournier M" first="Margot" last="Fournier">Margot Fournier</name></author><author><name sortKey="Roux, Amandine" sort="Roux, Amandine" uniqKey="Roux A" first="Amandine" last="Roux">Amandine Roux</name></author><author><name sortKey="Garrigue, Jerome" sort="Garrigue, Jerome" uniqKey="Garrigue J" first="Jérôme" last="Garrigue">Jérôme Garrigue</name></author><author><name sortKey="Muriel, Marie Paule" sort="Muriel, Marie Paule" uniqKey="Muriel M" first="Marie-Paule" last="Muriel">Marie-Paule Muriel</name></author><author><name sortKey="Blanche, Paul" sort="Blanche, Paul" uniqKey="Blanche P" first="Paul" last="Blanche">Paul Blanche</name></author><author><name sortKey="Lashuel, Hilal A" sort="Lashuel, Hilal A" uniqKey="Lashuel H" first="Hilal A" last="Lashuel">Hilal A. Lashuel</name></author><author><name sortKey="Anderson, John P" sort="Anderson, John P" uniqKey="Anderson J" first="John P" last="Anderson">John P. Anderson</name></author><author><name sortKey="Barbour, Robin" sort="Barbour, Robin" uniqKey="Barbour R" first="Robin" last="Barbour">Robin Barbour</name></author><author><name sortKey="Huang, Jiping" sort="Huang, Jiping" uniqKey="Huang J" first="Jiping" last="Huang">Jiping Huang</name></author><author><name sortKey="Du Montcel, Sophie Tezenas" sort="Du Montcel, Sophie Tezenas" uniqKey="Du Montcel S" first="Sophie Tezenas" last="Du Montcel">Sophie Tezenas Du Montcel</name></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name></author><author><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name><affiliation><nlm:affiliation>Inserm, U 975, CRICM, Hôpital de la Pitié-Salpêtrière, F-75013 Paris, France. olga.corti@upmc.fr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24192137</idno><idno type="pmid">24192137</idno><idno type="doi">10.1186/1471-2202-14-135</idno><idno type="wicri:Area/PubMed/Corpus">000664</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000664</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.</title><author><name sortKey="Fournier, Margot" sort="Fournier, Margot" uniqKey="Fournier M" first="Margot" last="Fournier">Margot Fournier</name></author><author><name sortKey="Roux, Amandine" sort="Roux, Amandine" uniqKey="Roux A" first="Amandine" last="Roux">Amandine Roux</name></author><author><name sortKey="Garrigue, Jerome" sort="Garrigue, Jerome" uniqKey="Garrigue J" first="Jérôme" last="Garrigue">Jérôme Garrigue</name></author><author><name sortKey="Muriel, Marie Paule" sort="Muriel, Marie Paule" uniqKey="Muriel M" first="Marie-Paule" last="Muriel">Marie-Paule Muriel</name></author><author><name sortKey="Blanche, Paul" sort="Blanche, Paul" uniqKey="Blanche P" first="Paul" last="Blanche">Paul Blanche</name></author><author><name sortKey="Lashuel, Hilal A" sort="Lashuel, Hilal A" uniqKey="Lashuel H" first="Hilal A" last="Lashuel">Hilal A. Lashuel</name></author><author><name sortKey="Anderson, John P" sort="Anderson, John P" uniqKey="Anderson J" first="John P" last="Anderson">John P. Anderson</name></author><author><name sortKey="Barbour, Robin" sort="Barbour, Robin" uniqKey="Barbour R" first="Robin" last="Barbour">Robin Barbour</name></author><author><name sortKey="Huang, Jiping" sort="Huang, Jiping" uniqKey="Huang J" first="Jiping" last="Huang">Jiping Huang</name></author><author><name sortKey="Du Montcel, Sophie Tezenas" sort="Du Montcel, Sophie Tezenas" uniqKey="Du Montcel S" first="Sophie Tezenas" last="Du Montcel">Sophie Tezenas Du Montcel</name></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name></author><author><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name><affiliation><nlm:affiliation>Inserm, U 975, CRICM, Hôpital de la Pitié-Salpêtrière, F-75013 Paris, France. olga.corti@upmc.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">BMC neuroscience</title><idno type="eISSN">1471-2202</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Disease Models, Animal</term><term>Fluorescent Antibody Technique</term><term>Humans</term><term>Mass Spectrometry</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Mice, Transgenic</term><term>Microscopy, Electron, Transmission</term><term>Motor Skills</term><term>Nerve Degeneration (genetics)</term><term>Nerve Degeneration (pathology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Ubiquitin-Protein Ligases (genetics)</term><term>alpha-Synuclein (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Disease Models, Animal</term><term>Fluorescent Antibody Technique</term><term>Humans</term><term>Mass Spectrometry</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Mice, Transgenic</term><term>Microscopy, Electron, Transmission</term><term>Motor Skills</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations of the gene encoding the major component of Lewy bodies (LB), α-synuclein (α-syn), cause autosomal dominant forms of Parkinson's disease (PD), whereas loss-of-function mutations of the gene encoding the multifunctional E3 ubiquitin-protein ligase Parkin account for autosomal recessive forms of the disease. Parkin overproduction protects against α-syn-dependent neurodegeneration in various in vitro and in vivo models, but it remains unclear whether this process is affected by Parkin deficiency. We addressed this issue, by carrying out more detailed analyses of transgenic mice overproducing the A30P variant of human α-syn (hA30Pα-syn) and with two, one or no parkin knockout alleles.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24192137</PMID><DateCreated><Year>2014</Year><Month>01</Month><Day>17</Day></DateCreated><DateCompleted><Year>2014</Year><Month>04</Month><Day>07</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>28</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2202</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><PubDate><Year>2013</Year><Month>Nov</Month><Day>05</Day></PubDate></JournalIssue><Title>BMC neuroscience</Title><ISOAbbreviation>BMC Neurosci</ISOAbbreviation></Journal><ArticleTitle>Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.</ArticleTitle><Pagination><MedlinePgn>135</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/1471-2202-14-135</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Mutations of the gene encoding the major component of Lewy bodies (LB), α-synuclein (α-syn), cause autosomal dominant forms of Parkinson's disease (PD), whereas loss-of-function mutations of the gene encoding the multifunctional E3 ubiquitin-protein ligase Parkin account for autosomal recessive forms of the disease. Parkin overproduction protects against α-syn-dependent neurodegeneration in various in vitro and in vivo models, but it remains unclear whether this process is affected by Parkin deficiency. We addressed this issue, by carrying out more detailed analyses of transgenic mice overproducing the A30P variant of human α-syn (hA30Pα-syn) and with two, one or no parkin knockout alleles.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Longitudinal behavioral follow-up of these mice indicated that Parkin depletion delayed disease-predictive sensorimotor impairment due to α-syn accumulation, in a dose-dependent fashion. At the end stage of the disease, neuronal deposits containing fibrillar α-syn species phosphorylated at S129 (PS129α-syn) were the predominant neuropathological feature in hA30Pα-syn mice, regardless of their parkin expression. Some of these deposits colocalized with the LB markers ubiquitin and α-syn truncated at D135 (α-synD135), indicating that PS129α-syn is subjected to secondary posttranslational modification (PTM); these features were not significantly affected by parkin dysfunction.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These findings suggest that Parkin deficiency acts as a protective modifier in α-syn-dependent neurodegeneration, without overtly affecting the composition and characteristics of α-syn deposits in end-stage disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fournier</LastName><ForeName>Margot</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Roux</LastName><ForeName>Amandine</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Garrigue</LastName><ForeName>Jérôme</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Muriel</LastName><ForeName>Marie-Paule</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>Blanche</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Lashuel</LastName><ForeName>Hilal A</ForeName><Initials>HA</Initials></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>John P</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Barbour</LastName><ForeName>Robin</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Jiping</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>du Montcel</LastName><ForeName>Sophie Tezenas</ForeName><Initials>ST</Initials></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>Alexis</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Corti</LastName><ForeName>Olga</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Inserm, U 975, CRICM, Hôpital de la Pitié-Salpêtrière, F-75013 Paris, France. olga.corti@upmc.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>11</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>BMC Neurosci</MedlineTA><NlmUniqueID>100966986</NlmUniqueID><ISSNLinking>1471-2202</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="C111567">parkin protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Science. 2000 Feb 18;287(5456):1265-9</RefSource><PMID Version="1">10678833</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2011 Nov 16;31(46):16884-94</RefSource><PMID Version="1">22090514</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2000 Aug 15;20(16):6021-9</RefSource><PMID Version="1">10934251</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2001 Jan;76(1):87-96</RefSource><PMID Version="1">11145981</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2001 Apr 15;10(9):919-26</RefSource><PMID Version="1">11309365</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2001 Oct;7(10):1144-50</RefSource><PMID Version="1">11590439</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2001 Dec;159(6):2215-25</RefSource><PMID Version="1">11733371</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2001 Dec 15;21(24):9549-60</RefSource><PMID Version="1">11739566</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Cell Biol. 2002 Feb;4(2):160-4</RefSource><PMID Version="1">11813001</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2002 May 16;34(4):521-33</RefSource><PMID Version="1">12062037</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8968-73</RefSource><PMID Version="1">12084935</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10813-8</RefSource><PMID Version="1">12122208</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2002 Nov;110(10):1429-39</RefSource><PMID Version="1">12438441</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2002 Dec 13;277(50):49071-6</RefSource><PMID Version="1">12377775</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2002 Dec 19;36(6):1007-19</RefSource><PMID Version="1">12495618</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2003 Mar 27;37(6):911-24</RefSource><PMID Version="1">12670421</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2003 Jul;163(1):91-100</RefSource><PMID Version="1">12819014</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2003 Sep 15;12(18):2277-91</RefSource><PMID Version="1">12915482</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2003 Nov 7;278(45):44405-11</RefSource><PMID Version="1">12923179</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>BMC Neurosci. 2004 Apr 16;5:14</RefSource><PMID Version="1">15090075</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2004 Oct;91(2):451-61</RefSource><PMID Version="1">15447678</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 1998 Apr;152(4):879-84</RefSource><PMID Version="1">9546347</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochemistry. 2005 Jan 11;44(1):361-8</RefSource><PMID Version="1">15628878</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2005 Feb 8;102(6):2162-7</RefSource><PMID Version="1">15684072</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2005 Jun 17;280(24):22670-8</RefSource><PMID Version="1">15840579</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2006 Apr 5;26(14):3685-96</RefSource><PMID Version="1">16597723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 Oct 6;281(40):29739-52</RefSource><PMID Version="1">16847063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2007 Mar;130(Pt 3):799-815</RefSource><PMID Version="1">17303591</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neural Transm (Vienna). 2007;114(12):1509-17</RefSource><PMID Version="1">17576511</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Feb 8;283(6):3316-28</RefSource><PMID Version="1">18070888</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2008 Jun 13;283(24):16895-905</RefSource><PMID Version="1">18343814</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2009 Jan 30;284(5):2598-602</RefSource><PMID Version="1">19004816</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Methods Mol Biol. 2009;527:57-66, xi</RefSource><PMID Version="1">19241005</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2009;4(8):e6629</RefSource><PMID Version="1">19680561</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2009 Nov;119(11):3257-65</RefSource><PMID Version="1">19855133</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2010 Jan 22;285(4):2807-22</RefSource><PMID Version="1">19889641</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2010;25 Suppl 1:S32-9</RefSource><PMID Version="1">20187240</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Bioenerg Biomembr. 2010 Feb;42(1):85-95</RefSource><PMID Version="1">20148295</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2010;183:115-45</RefSource><PMID Version="1">20696318</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neuropathol Exp Neurol. 2010 Sep;69(9):959-72</RefSource><PMID Version="1">20720502</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2011 Mar 25;286(12):10814-24</RefSource><PMID Version="1">21252228</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Physiol Rev. 2011 Oct;91(4):1161-218</RefSource><PMID Version="1">22013209</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 2000 May 25;342(21):1560-7</RefSource><PMID Version="1">10824074</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005455" MajorTopicYN="N">Fluorescent Antibody Technique</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013058" MajorTopicYN="N">Mass Spectrometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D046529" MajorTopicYN="N">Microscopy, Electron, Transmission</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009048" MajorTopicYN="N">Motor Skills</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4228309</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>05</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>4</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24192137</ArticleId><ArticleId IdType="pii">1471-2202-14-135</ArticleId><ArticleId IdType="doi">10.1186/1471-2202-14-135</ArticleId><ArticleId IdType="pmc">PMC4228309</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000664 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 000664 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:24192137
|texte= Parkin depletion delays motor decline dose-dependently without overtly affecting neuropathology in α-synuclein transgenic mice.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:24192137" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |