Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.
Identifieur interne : 000976 ( PubMed/Checkpoint ); précédent : 000975; suivant : 000977Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.
Auteurs : Jesse R. Mclean [États-Unis] ; Penelope J. Hallett ; Oliver Cooper ; Michael Stanley ; Ole IsacsonSource :
- Molecular and cellular neurosciences [ 1095-9327 ] ; 2012.
English descriptors
- KwdEn :
- Alternative Splicing (genetics), Amino Acid Sequence, Animals, Cerebellum (metabolism), Disease Models, Animal, Gene Expression, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Neurons (metabolism), Parkinson Disease (genetics), Substantia Nigra (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , genetics : alpha-Synuclein.
- genetics : Alternative Splicing, Parkinson Disease.
- metabolism : Cerebellum, Neurons, Substantia Nigra, alpha-Synuclein.
- Amino Acid Sequence, Animals, Disease Models, Animal, Gene Expression, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data.
Abstract
Alternative splicing is a complex post-transcriptional process that can be regulated by cis-acting elements located within genomic non-coding regions. Recent studies have identified that polymorphic variations in non-coding regions of the α-synuclein gene (SNCA) locus are associated with an increased risk for developing Parkinson's disease (PD). The underlying mechanism(s) for this susceptibility may involve changes in α-synuclein mRNA expression and alternative splicing. As a first step towards understanding the biology of α-synuclein splice variants in PD, we characterized the levels of the full-length SNCA-140 mRNA transcript and SNCA-126, -112, and -98 alternatively spliced variants in different neuronal regions from PD patients or transgenic mice overexpressing human α-synuclein (ASO). In human post-mortem tissue, α-synuclein spliced transcripts were expressed in a region-specific manner in the cortex, substantia nigra, and cerebellum. We observed increased nigral SNCA-140 and SNCA-126 transcript levels in PD patients when compared to neurologically unaffected cases. Human α-synuclein splicing changes were also found to occur in a region-specific manner in ASO mice. Here, SNCA-126, -112, and -98 transcript levels did not increase proportionally with SNCA-140 levels, or parallel the region-specific mouse transcript ratios seen in wild-type (WT) littermates. While most transcripts were elevated in ASO mice when compared to WT mice, the most prominent increase was found in the ventral midbrain of 15-month-old ASO mice. These results demonstrate region-specific human α-synuclein transcript level abnormalities in PD patients and in a transgenic mouse model of α-synucleinopathy. This study is relevant to understanding the normal, adaptive, or pathological role(s) of α-synuclein splice variants.
DOI: 10.1016/j.mcn.2011.11.006
PubMed: 22155155
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:22155155Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.</title><author><name sortKey="Mclean, Jesse R" sort="Mclean, Jesse R" uniqKey="Mclean J" first="Jesse R" last="Mclean">Jesse R. Mclean</name><affiliation wicri:level="4"><nlm:affiliation>Center for Neuroregeneration Research, McLean Hospital/Harvard Medical School, Harvard University, MRC130, Belmont, MA 02478, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuroregeneration Research, McLean Hospital/Harvard Medical School, Harvard University, MRC130, Belmont, MA 02478</wicri:regionArea><placeName><region type="state">Massachusetts</region><settlement type="city">Cambridge (Massachusetts)</settlement></placeName><orgName type="university">Université Harvard</orgName></affiliation></author><author><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J" last="Hallett">Penelope J. Hallett</name></author><author><name sortKey="Cooper, Oliver" sort="Cooper, Oliver" uniqKey="Cooper O" first="Oliver" last="Cooper">Oliver Cooper</name></author><author><name sortKey="Stanley, Michael" sort="Stanley, Michael" uniqKey="Stanley M" first="Michael" last="Stanley">Michael Stanley</name></author><author><name sortKey="Isacson, Ole" sort="Isacson, Ole" uniqKey="Isacson O" first="Ole" last="Isacson">Ole Isacson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22155155</idno><idno type="pmid">22155155</idno><idno type="doi">10.1016/j.mcn.2011.11.006</idno><idno type="wicri:Area/PubMed/Corpus">000B07</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000B07</idno><idno type="wicri:Area/PubMed/Curation">000B07</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000B07</idno><idno type="wicri:Area/PubMed/Checkpoint">000B07</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000B07</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.</title><author><name sortKey="Mclean, Jesse R" sort="Mclean, Jesse R" uniqKey="Mclean J" first="Jesse R" last="Mclean">Jesse R. Mclean</name><affiliation wicri:level="4"><nlm:affiliation>Center for Neuroregeneration Research, McLean Hospital/Harvard Medical School, Harvard University, MRC130, Belmont, MA 02478, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuroregeneration Research, McLean Hospital/Harvard Medical School, Harvard University, MRC130, Belmont, MA 02478</wicri:regionArea><placeName><region type="state">Massachusetts</region><settlement type="city">Cambridge (Massachusetts)</settlement></placeName><orgName type="university">Université Harvard</orgName></affiliation></author><author><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J" last="Hallett">Penelope J. Hallett</name></author><author><name sortKey="Cooper, Oliver" sort="Cooper, Oliver" uniqKey="Cooper O" first="Oliver" last="Cooper">Oliver Cooper</name></author><author><name sortKey="Stanley, Michael" sort="Stanley, Michael" uniqKey="Stanley M" first="Michael" last="Stanley">Michael Stanley</name></author><author><name sortKey="Isacson, Ole" sort="Isacson, Ole" uniqKey="Isacson O" first="Ole" last="Isacson">Ole Isacson</name></author></analytic><series><title level="j">Molecular and cellular neurosciences</title><idno type="eISSN">1095-9327</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alternative Splicing (genetics)</term><term>Amino Acid Sequence</term><term>Animals</term><term>Cerebellum (metabolism)</term><term>Disease Models, Animal</term><term>Gene Expression</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Molecular Sequence Data</term><term>Neurons (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Substantia Nigra (metabolism)</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Alternative Splicing</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebellum</term><term>Neurons</term><term>Substantia Nigra</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Disease Models, Animal</term><term>Gene Expression</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Molecular Sequence Data</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alternative splicing is a complex post-transcriptional process that can be regulated by cis-acting elements located within genomic non-coding regions. Recent studies have identified that polymorphic variations in non-coding regions of the α-synuclein gene (SNCA) locus are associated with an increased risk for developing Parkinson's disease (PD). The underlying mechanism(s) for this susceptibility may involve changes in α-synuclein mRNA expression and alternative splicing. As a first step towards understanding the biology of α-synuclein splice variants in PD, we characterized the levels of the full-length SNCA-140 mRNA transcript and SNCA-126, -112, and -98 alternatively spliced variants in different neuronal regions from PD patients or transgenic mice overexpressing human α-synuclein (ASO). In human post-mortem tissue, α-synuclein spliced transcripts were expressed in a region-specific manner in the cortex, substantia nigra, and cerebellum. We observed increased nigral SNCA-140 and SNCA-126 transcript levels in PD patients when compared to neurologically unaffected cases. Human α-synuclein splicing changes were also found to occur in a region-specific manner in ASO mice. Here, SNCA-126, -112, and -98 transcript levels did not increase proportionally with SNCA-140 levels, or parallel the region-specific mouse transcript ratios seen in wild-type (WT) littermates. While most transcripts were elevated in ASO mice when compared to WT mice, the most prominent increase was found in the ventral midbrain of 15-month-old ASO mice. These results demonstrate region-specific human α-synuclein transcript level abnormalities in PD patients and in a transgenic mouse model of α-synucleinopathy. This study is relevant to understanding the normal, adaptive, or pathological role(s) of α-synuclein splice variants.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22155155</PMID><DateCreated><Year>2012</Year><Month>02</Month><Day>13</Day></DateCreated><DateCompleted><Year>2012</Year><Month>06</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-9327</ISSN><JournalIssue CitedMedium="Internet"><Volume>49</Volume><Issue>2</Issue><PubDate><Year>2012</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Molecular and cellular neurosciences</Title><ISOAbbreviation>Mol. Cell. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.</ArticleTitle><Pagination><MedlinePgn>230-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.mcn.2011.11.006</ELocationID><Abstract><AbstractText>Alternative splicing is a complex post-transcriptional process that can be regulated by cis-acting elements located within genomic non-coding regions. Recent studies have identified that polymorphic variations in non-coding regions of the α-synuclein gene (SNCA) locus are associated with an increased risk for developing Parkinson's disease (PD). The underlying mechanism(s) for this susceptibility may involve changes in α-synuclein mRNA expression and alternative splicing. As a first step towards understanding the biology of α-synuclein splice variants in PD, we characterized the levels of the full-length SNCA-140 mRNA transcript and SNCA-126, -112, and -98 alternatively spliced variants in different neuronal regions from PD patients or transgenic mice overexpressing human α-synuclein (ASO). In human post-mortem tissue, α-synuclein spliced transcripts were expressed in a region-specific manner in the cortex, substantia nigra, and cerebellum. We observed increased nigral SNCA-140 and SNCA-126 transcript levels in PD patients when compared to neurologically unaffected cases. Human α-synuclein splicing changes were also found to occur in a region-specific manner in ASO mice. Here, SNCA-126, -112, and -98 transcript levels did not increase proportionally with SNCA-140 levels, or parallel the region-specific mouse transcript ratios seen in wild-type (WT) littermates. While most transcripts were elevated in ASO mice when compared to WT mice, the most prominent increase was found in the ventral midbrain of 15-month-old ASO mice. These results demonstrate region-specific human α-synuclein transcript level abnormalities in PD patients and in a transgenic mouse model of α-synucleinopathy. This study is relevant to understanding the normal, adaptive, or pathological role(s) of α-synuclein splice variants.</AbstractText><CopyrightInformation>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>McLean</LastName><ForeName>Jesse R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Center for Neuroregeneration Research, McLean Hospital/Harvard Medical School, Harvard University, MRC130, Belmont, MA 02478, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hallett</LastName><ForeName>Penelope J</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Cooper</LastName><ForeName>Oliver</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Stanley</LastName><ForeName>Michael</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Isacson</LastName><ForeName>Ole</ForeName><Initials>O</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R24 MH068855-10</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS39793</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>P50 NS039793</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS039793-10</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R24 MH068855</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>12</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell Neurosci</MedlineTA><NlmUniqueID>9100095</NlmUniqueID><ISSNLinking>1044-7431</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497604">SNCA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neuroreport. 2006 Aug 21;17(12):1327-30</RefSource><PMID Version="1">16951579</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neuropathol. 2006 Sep;112(3):237-51</RefSource><PMID Version="1">16845533</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2007 Jan;25(1):134-49</RefSource><PMID Version="1">17055279</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci Res. 2007 May 15;85(7):1538-46</RefSource><PMID Version="1">17387688</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2007 Dec;61(12):991-1001</RefSource><PMID Version="1">17879265</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Front Biosci. 2008;13:867-78</RefSource><PMID Version="1">17981595</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurogenetics. 2008 Feb;9(1):15-23</RefSource><PMID Version="1">17955272</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2007;13 Suppl 3:S309-15</RefSource><PMID Version="1">18267256</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2008 Apr;36(7):e38</RefSource><PMID Version="1">18332041</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>RNA. 2008 May;14(5):802-13</RefSource><PMID Version="1">18369186</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2008 May;22(5):1327-34</RefSource><PMID Version="1">18162487</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurogenetics. 2008 Jul;9(3):163-72</RefSource><PMID Version="1">18335262</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nucleic Acids Res. 2008 Sep;36(15):4823-32</RefSource><PMID Version="1">18653532</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2008 Oct;107(2):303-16</RefSource><PMID Version="1">18691382</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2009 Jan;66(1):32-8</RefSource><PMID Version="1">19139297</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2009 Feb;23(2):329-40</RefSource><PMID Version="1">18948383</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2009 Jul;1792(7):597-603</RefSource><PMID Version="1">19063963</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2009 Sep 1;18(17):3274-85</RefSource><PMID Version="1">19498036</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Protein Pept Sci. 2009 Oct;10(5):476-82</RefSource><PMID Version="1">19538156</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2009 Dec;220(2):359-65</RefSource><PMID Version="1">19800328</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2009 Dec;41(12):1308-12</RefSource><PMID Version="1">19915575</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2009 Dec;41(12):1303-7</RefSource><PMID Version="1">19915576</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2010 Feb;221(2):267-74</RefSource><PMID Version="1">19944097</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 2010 Feb 1;48(3):377-83</RefSource><PMID Version="1">19857570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2010 Apr;133(Pt 4):957-72</RefSource><PMID Version="1">20150322</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Genet. 2010 May;11(5):345-55</RefSource><PMID Version="1">20376054</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2010 May 6;465(7294):53-9</RefSource><PMID Version="1">20445623</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mutat. 2010 Jul;31(7):763-80</RefSource><PMID Version="1">20506312</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Brain Res. 2010;183:115-45</RefSource><PMID Version="1">20696318</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurotoxicology. 2010 Sep;31(5):598-602</RefSource><PMID Version="1">20430055</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Cell Dev Biol. 2010;26:211-33</RefSource><PMID Version="1">20500090</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2010 Sep 24;329(5999):1663-7</RefSource><PMID Version="1">20798282</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurogenetics. 2011 Feb;12(1):59-64</RefSource><PMID Version="1">21046180</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2000;920:16-27</RefSource><PMID Version="1">11193145</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2001 Dec 15;10(26):3101-9</RefSource><PMID Version="1">11751692</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2002 May 3;323(3):219-23</RefSource><PMID Version="1">11959424</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci Res. 2002 Jun 1;68(5):568-78</RefSource><PMID Version="1">12111846</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biomol Struct Dyn. 2003 Oct;21(2):211-34</RefSource><PMID Version="1">12956606</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2004 Apr;186(2):158-72</RefSource><PMID Version="1">15026254</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2004 Nov;17(2):123-30</RefSource><PMID Version="1">15474350</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1988 Aug;8(8):2804-15</RefSource><PMID Version="1">3411354</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11282-6</RefSource><PMID Version="1">8248242</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 1994 Dec 15;205(2):1366-72</RefSource><PMID Version="1">7802671</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 1995 Feb;14(2):467-75</RefSource><PMID Version="1">7857654</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genomics. 1995 Mar 20;26(2):254-7</RefSource><PMID Version="1">7601450</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 1998 Apr 17;273(16):9443-9</RefSource><PMID Version="1">9545270</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 1999 May;14(3):417-22</RefSource><PMID Version="1">10348463</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 1999;91(2):651-9</RefSource><PMID Version="1">10366022</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Res. 2004 Nov 1;64(21):7647-54</RefSource><PMID Version="1">15520162</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Physiol Pharmacol. 2005 Mar;56(1):29-37</RefSource><PMID Version="1">15795473</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Med Genet. 2005 Oct;42(10):737-48</RefSource><PMID Version="1">16199547</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2006 Oct;21(10):1703-8</RefSource><PMID Version="1">16795004</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D017398" MajorTopicYN="N">Alternative Splicing</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002531" MajorTopicYN="N">Cerebellum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</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="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS343015</OtherID><OtherID Source="NLM">PMC3340908</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>07</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>11</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>6</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22155155</ArticleId><ArticleId IdType="pii">S1044-7431(11)00262-4</ArticleId><ArticleId IdType="doi">10.1016/j.mcn.2011.11.006</ArticleId><ArticleId IdType="pmc">PMC3340908</ArticleId><ArticleId IdType="mid">NIHMS343015</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region><settlement><li>Cambridge (Massachusetts)</li></settlement><orgName><li>Université Harvard</li></orgName></list><tree><noCountry><name sortKey="Cooper, Oliver" sort="Cooper, Oliver" uniqKey="Cooper O" first="Oliver" last="Cooper">Oliver Cooper</name><name sortKey="Hallett, Penelope J" sort="Hallett, Penelope J" uniqKey="Hallett P" first="Penelope J" last="Hallett">Penelope J. Hallett</name><name sortKey="Isacson, Ole" sort="Isacson, Ole" uniqKey="Isacson O" first="Ole" last="Isacson">Ole Isacson</name><name sortKey="Stanley, Michael" sort="Stanley, Michael" uniqKey="Stanley M" first="Michael" last="Stanley">Michael Stanley</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Mclean, Jesse R" sort="Mclean, Jesse R" uniqKey="Mclean J" first="Jesse R" last="Mclean">Jesse R. Mclean</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PubMed/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000976 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 000976 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= PubMed
|étape= Checkpoint
|type= RBID
|clé= pubmed:22155155
|texte= Transcript expression levels of full-length alpha-synuclein and its three alternatively spliced variants in Parkinson's disease brain regions and in a transgenic mouse model of alpha-synuclein overexpression.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:22155155" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |