PittsburghV1, PubMed, Checkpoint, bibRecord, 003135

ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.

Identifieur interne : 003135 ( PubMed/Checkpoint ); précédent : 003134; suivant : 003136

ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.

Auteurs : Manish Verma [États-Unis] ; Erin K. Steer [États-Unis] ; Charleen T. Chu [États-Unis]

Source :

Biochimica et biophysica acta [ 0006-3002 ] ; 2014.

RBID : pubmed:24225420

Descripteurs français

KwdFr :
- Animaux, Extracellular Signal-Regulated MAP Kinases (métabolisme), Humains, Maladie de Parkinson (anatomopathologie), Maladie de Parkinson (enzymologie), Maladie de Parkinson (génétique), Modèles biologiques, Mutation (génétique), Protein-Serine-Threonine Kinases (génétique), Protein-Serine-Threonine Kinases (métabolisme), Voie de signalisation Wnt.
MESH :
- anatomopathologie : Maladie de Parkinson.
- enzymologie : Maladie de Parkinson.
- génétique : Maladie de Parkinson, Mutation, Protein-Serine-Threonine Kinases.
- métabolisme : Extracellular Signal-Regulated MAP Kinases, Protein-Serine-Threonine Kinases.
- Animaux, Humains, Modèles biologiques, Voie de signalisation Wnt.

English descriptors

KwdEn :
- Animals, Extracellular Signal-Regulated MAP Kinases (metabolism), Humans, Models, Biological, Mutation (genetics), Parkinson Disease (enzymology), Parkinson Disease (genetics), Parkinson Disease (pathology), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Wnt Signaling Pathway.
MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Extracellular Signal-Regulated MAP Kinases, Protein-Serine-Threonine Kinases.
- enzymology : Parkinson Disease.
- genetics : Mutation, Parkinson Disease.
- pathology : Parkinson Disease.
- Animals, Humans, Models, Biological, Wnt Signaling Pathway.

Abstract

The leucine rich repeat kinase 2 (LRRK2/dardarin) is implicated in autosomal dominant familial and sporadic Parkinson's disease (PD); mutations in LRRK2 account for up to 40% of PD cases in some populations. LRRK2 is a large protein with a kinase domain, a GTPase domain, and multiple potential protein interaction domains. As such, delineating the functional pathways for LRRK2 and mechanisms by which PD-linked variants contribute to age-related neurodegeneration could result in pharmaceutically tractable therapies. A growing number of recent studies implicate dysregulation of mitogen activated protein kinases 3 and 1 (also known as ERK1/2) as possible downstream mediators of mutant LRRK2 effects. As these master regulators of growth, differentiation, neuronal plasticity and cell survival have also been implicated in other PD models, a set of common cell biological pathways may contribute to neuronal susceptibility in PD. Here, we review the literature on several major cellular pathways impacted by LRRK2 mutations--autophagy, microtubule/cytoskeletal dynamics, and protein synthesis--in context of potential signaling crosstalk involving the ERK1/2 and Wnt signaling pathways. Emerging implications for calcium homeostasis, mitochondrial biology and synaptic dysregulation are discussed in relation to LRRK2 interactions with other PD gene products. It has been shown that substantia nigra neurons in human PD and Lewy body dementia patients exhibit cytoplasmic accumulations of ERK1/2 in mitochondria, autophagosomes and bundles of intracellular fibrils. Both experimental and human tissue data implicate pathogenic changes in ERK1/2 signaling in sporadic, toxin-based and mutant LRRK2 settings, suggesting engagement of common cell biological pathways by divergent PD etiologies.

DOI: 10.1016/j.bbadis.2013.11.005
PubMed: 24225420

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 002137
to stream PubMed, to step Curation: 002128

Links to Exploration step

pubmed:24225420

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.</title>
<author><name sortKey="Verma, Manish" sort="Verma, Manish" uniqKey="Verma M" first="Manish" last="Verma">Manish Verma</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Steer, Erin K" sort="Steer, Erin K" uniqKey="Steer E" first="Erin K" last="Steer">Erin K. Steer</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chu, Charleen T" sort="Chu, Charleen T" uniqKey="Chu C" first="Charleen T" last="Chu">Charleen T. Chu</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: ctc4@pitt.edu.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2014">2014</date>
<idno type="RBID">pubmed:24225420</idno>
<idno type="pmid">24225420</idno>
<idno type="doi">10.1016/j.bbadis.2013.11.005</idno>
<idno type="wicri:Area/PubMed/Corpus">002137</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002137</idno>
<idno type="wicri:Area/PubMed/Curation">002128</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002128</idno>
<idno type="wicri:Area/PubMed/Checkpoint">002128</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">002128</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.</title>
<author><name sortKey="Verma, Manish" sort="Verma, Manish" uniqKey="Verma M" first="Manish" last="Verma">Manish Verma</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Steer, Erin K" sort="Steer, Erin K" uniqKey="Steer E" first="Erin K" last="Steer">Erin K. Steer</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chu, Charleen T" sort="Chu, Charleen T" uniqKey="Chu C" first="Charleen T" last="Chu">Charleen T. Chu</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: ctc4@pitt.edu.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213</wicri:regionArea>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Biochimica et biophysica acta</title>
<idno type="ISSN">0006-3002</idno>
<imprint><date when="2014" type="published">2014</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Extracellular Signal-Regulated MAP Kinases (metabolism)</term>
<term>Humans</term>
<term>Models, Biological</term>
<term>Mutation (genetics)</term>
<term>Parkinson Disease (enzymology)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Wnt Signaling Pathway</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term>
<term>Humains</term>
<term>Maladie de Parkinson (anatomopathologie)</term>
<term>Maladie de Parkinson (enzymologie)</term>
<term>Maladie de Parkinson (génétique)</term>
<term>Modèles biologiques</term>
<term>Mutation (génétique)</term>
<term>Protein-Serine-Threonine Kinases (génétique)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Voie de signalisation Wnt</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladie de Parkinson</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Maladie de Parkinson</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Mutation</term>
<term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Models, Biological</term>
<term>Wnt Signaling Pathway</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Modèles biologiques</term>
<term>Voie de signalisation Wnt</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The leucine rich repeat kinase 2 (LRRK2/dardarin) is implicated in autosomal dominant familial and sporadic Parkinson's disease (PD); mutations in LRRK2 account for up to 40% of PD cases in some populations. LRRK2 is a large protein with a kinase domain, a GTPase domain, and multiple potential protein interaction domains. As such, delineating the functional pathways for LRRK2 and mechanisms by which PD-linked variants contribute to age-related neurodegeneration could result in pharmaceutically tractable therapies. A growing number of recent studies implicate dysregulation of mitogen activated protein kinases 3 and 1 (also known as ERK1/2) as possible downstream mediators of mutant LRRK2 effects. As these master regulators of growth, differentiation, neuronal plasticity and cell survival have also been implicated in other PD models, a set of common cell biological pathways may contribute to neuronal susceptibility in PD. Here, we review the literature on several major cellular pathways impacted by LRRK2 mutations--autophagy, microtubule/cytoskeletal dynamics, and protein synthesis--in context of potential signaling crosstalk involving the ERK1/2 and Wnt signaling pathways. Emerging implications for calcium homeostasis, mitochondrial biology and synaptic dysregulation are discussed in relation to LRRK2 interactions with other PD gene products. It has been shown that substantia nigra neurons in human PD and Lewy body dementia patients exhibit cytoplasmic accumulations of ERK1/2 in mitochondria, autophagosomes and bundles of intracellular fibrils. Both experimental and human tissue data implicate pathogenic changes in ERK1/2 signaling in sporadic, toxin-based and mutant LRRK2 settings, suggesting engagement of common cell biological pathways by divergent PD etiologies.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24225420</PMID>
<DateCreated><Year>2014</Year>
<Month>06</Month>
<Day>30</Day>
</DateCreated>
<DateCompleted><Year>2014</Year>
<Month>09</Month>
<Day>03</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>02</Month>
<Day>20</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-3002</ISSN>
<JournalIssue CitedMedium="Print"><Volume>1842</Volume>
<Issue>8</Issue>
<PubDate><Year>2014</Year>
<Month>Aug</Month>
</PubDate>
</JournalIssue>
<Title>Biochimica et biophysica acta</Title>
<ISOAbbreviation>Biochim. Biophys. Acta</ISOAbbreviation>
</Journal>
<ArticleTitle>ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>1273-81</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbadis.2013.11.005</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0925-4439(13)00330-X</ELocationID>
<Abstract><AbstractText>The leucine rich repeat kinase 2 (LRRK2/dardarin) is implicated in autosomal dominant familial and sporadic Parkinson's disease (PD); mutations in LRRK2 account for up to 40% of PD cases in some populations. LRRK2 is a large protein with a kinase domain, a GTPase domain, and multiple potential protein interaction domains. As such, delineating the functional pathways for LRRK2 and mechanisms by which PD-linked variants contribute to age-related neurodegeneration could result in pharmaceutically tractable therapies. A growing number of recent studies implicate dysregulation of mitogen activated protein kinases 3 and 1 (also known as ERK1/2) as possible downstream mediators of mutant LRRK2 effects. As these master regulators of growth, differentiation, neuronal plasticity and cell survival have also been implicated in other PD models, a set of common cell biological pathways may contribute to neuronal susceptibility in PD. Here, we review the literature on several major cellular pathways impacted by LRRK2 mutations--autophagy, microtubule/cytoskeletal dynamics, and protein synthesis--in context of potential signaling crosstalk involving the ERK1/2 and Wnt signaling pathways. Emerging implications for calcium homeostasis, mitochondrial biology and synaptic dysregulation are discussed in relation to LRRK2 interactions with other PD gene products. It has been shown that substantia nigra neurons in human PD and Lewy body dementia patients exhibit cytoplasmic accumulations of ERK1/2 in mitochondria, autophagosomes and bundles of intracellular fibrils. Both experimental and human tissue data implicate pathogenic changes in ERK1/2 signaling in sporadic, toxin-based and mutant LRRK2 settings, suggesting engagement of common cell biological pathways by divergent PD etiologies.</AbstractText>
<CopyrightInformation>Copyright © 2013 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Verma</LastName>
<ForeName>Manish</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Steer</LastName>
<ForeName>Erin K</ForeName>
<Initials>EK</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chu</LastName>
<ForeName>Charleen T</ForeName>
<Initials>CT</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: ctc4@pitt.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P50 NS040256</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AG026389</GrantID>
<Acronym>AG</Acronym>
<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 NS065789</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R56 NS065789</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>11</Month>
<Day>10</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Biochim Biophys Acta</MedlineTA>
<NlmUniqueID>0217513</NlmUniqueID>
<ISSNLinking>0006-3002</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
<NameOfSubstance UI="D048049">Extracellular Signal-Regulated MAP Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Environ Health Perspect. 1996 Jun;104(6):652-4</RefSource>
<PMID Version="1">8793354</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 2010 Aug 23;190(4):533-9</RefSource>
<PMID Version="1">20713600</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Chem Biol. 2011 Apr;7(4):203-5</RefSource>
<PMID Version="1">21378983</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuron. 2012 Sep 20;75(6):1008-21</RefSource>
<PMID Version="1">22998870</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2011 Feb 9;31(6):2225-37</RefSource>
<PMID Version="1">21307259</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2008 May;105(3):1048-56</RefSource>
<PMID Version="1">18182054</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2011 Jul;43(1):60-7</RefSource>
<PMID Version="1">20969957</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2009 Oct 6;163(2):533-9</RefSource>
<PMID Version="1">19559761</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>EMBO J. 2008 Sep 17;27(18):2432-43</RefSource>
<PMID Version="1">18701920</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2009 Nov 15;18(22):4390-404</RefSource>
<PMID Version="1">19692353</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Nov 15;21(22):4966-79</RefSource>
<PMID Version="1">22899650</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain Pathol. 2003 Oct;13(4):473-81</RefSource>
<PMID Version="1">14655753</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Feb 1;21(3):511-25</RefSource>
<PMID Version="1">22012985</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2007 Jan;22(1):55-61</RefSource>
<PMID Version="1">17115391</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Exp Cell Res. 2010 Feb 15;316(4):649-56</RefSource>
<PMID Version="1">19769964</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Dev Neurosci. 2005 Mar-Aug;27(2-4):93-9</RefSource>
<PMID Version="1">16046842</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2005 Oct 7;280(40):34105-12</RefSource>
<PMID Version="1">16091364</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2012;7(5):e36191</RefSource>
<PMID Version="1">22563483</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci Res. 2007 May 1;85(6):1288-94</RefSource>
<PMID Version="1">17385669</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2012;7(10):e47784</RefSource>
<PMID Version="1">23082216</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Neurodegener. 2012;7:2</RefSource>
<PMID Version="1">22230652</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2013 Mar;182(3):612-22</RefSource>
<PMID Version="1">23369575</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>ASN Neuro. 2009;1(1). pii: e00002. doi: 10.1042/AN20090007</RefSource>
<PMID Version="1">19570025</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Geriatr Psychiatry Neurol. 2010 Dec;23(4):228-42</RefSource>
<PMID Version="1">20938043</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Oct 1;21(19):4201-13</RefSource>
<PMID Version="1">22736029</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Mol Endocrinol. 2003 Apr;30(2):117-26</RefSource>
<PMID Version="1">12683936</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2008 Jan;118(1):149-60</RefSource>
<PMID Version="1">18060047</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Trends Neurosci. 2006 May;29(5):286-93</RefSource>
<PMID Version="1">16616379</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12747-52</RefSource>
<PMID Version="1">14557550</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2001 May;77(4):1058-66</RefSource>
<PMID Version="1">11359871</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Science. 1995 Nov 24;270(5240):1326-31</RefSource>
<PMID Version="1">7481820</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuropathol Appl Neurobiol. 2010 Apr;36(2):125-32</RefSource>
<PMID Version="1">20202120</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2000 Dec;3(12):1301-6</RefSource>
<PMID Version="1">11100151</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Science. 2010 Dec 3;330(6009):1344-8</RefSource>
<PMID Version="1">21127245</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 1992 Jul;42(7):1328-35</RefSource>
<PMID Version="1">1620342</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2007 Jan;170(1):75-86</RefSource>
<PMID Version="1">17200184</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Lancet. 2005 Jan 29-Feb 4;365(9457):415-6</RefSource>
<PMID Version="1">15680457</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Science. 1994 Oct 14;266(5183):282-5</RefSource>
<PMID Version="1">7939665</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2009 Sep;110(5):1514-22</RefSource>
<PMID Version="1">19545277</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Signal. 2010 May;22(5):821-7</RefSource>
<PMID Version="1">20074637</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Pathol. 2010 May;221(1):3-12</RefSource>
<PMID Version="1">20225336</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2012 Aug;122(3):650-8</RefSource>
<PMID Version="1">22639965</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Cell Biol. 2007 Nov;27(21):7486-96</RefSource>
<PMID Version="1">17709391</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2010 Dec;40(3):503-17</RefSource>
<PMID Version="1">20659558</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuron. 2006 Nov 22;52(4):587-93</RefSource>
<PMID Version="1">17114044</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain Pathol. 2003 Jan;13(1):62-78</RefSource>
<PMID Version="1">12580546</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem J. 2009 Nov 15;424(1):47-60</RefSource>
<PMID Version="1">19740074</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Curr Top Dev Biol. 2011;97:21-53</RefSource>
<PMID Version="1">22074601</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 Jun 16;281(24):16436-42</RefSource>
<PMID Version="1">16621802</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2009 Mar;108(6):1561-74</RefSource>
<PMID Version="1">19166511</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2010 May 25;107(21):9879-84</RefSource>
<PMID Version="1">20457918</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Genes Dev. 1997 Dec 15;11(24):3286-305</RefSource>
<PMID Version="1">9407023</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2004 Nov;91(3):667-82</RefSource>
<PMID Version="1">15485497</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Mol Life Sci. 2013 Jan;70(1):121-36</RefSource>
<PMID Version="1">22773119</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2002 May 10;935(1-2):32-9</RefSource>
<PMID Version="1">12062470</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2012 May 30;32(22):7585-93</RefSource>
<PMID Version="1">22649237</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2009;4(5):e5701</RefSource>
<PMID Version="1">19492085</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Struct Mol Biol. 2005 Sep;12(9):772-8</RefSource>
<PMID Version="1">16116436</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neural Transm (Vienna). 2001;108(12):1383-96</RefSource>
<PMID Version="1">11810403</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2009 May;109(4):959-68</RefSource>
<PMID Version="1">19302196</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2010 Jul 30;1346:26-42</RefSource>
<PMID Version="1">20513370</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2009 Nov 1;18(21):4022-34</RefSource>
<PMID Version="1">19640926</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Tissue Res. 2004 Oct;318(1):121-34</RefSource>
<PMID Version="1">15338272</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biosci. 2003 Feb;28(1):83-9</RefSource>
<PMID Version="1">12682429</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell. 1986 May 9;45(3):329-42</RefSource>
<PMID Version="1">3516413</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Calcium. 2011 May;49(5):296-305</RefSource>
<PMID Version="1">21163523</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Death Differ. 2000 Oct;7(10):861-5</RefSource>
<PMID Version="1">11279530</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 2009 Mar 13;33(5):627-38</RefSource>
<PMID Version="1">19285945</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2010 Dec 15;30(50):16959-69</RefSource>
<PMID Version="1">21159966</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2010;5(1):e8730</RefSource>
<PMID Version="1">20090955</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16842-7</RefSource>
<PMID Version="1">16269541</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2013 Feb;182(2):474-84</RefSource>
<PMID Version="1">23231918</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS Genet. 2010 Apr;6(4):e1000902</RefSource>
<PMID Version="1">20386743</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1993 Oct;61(4):1191-206</RefSource>
<PMID Version="1">8376979</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2002 Mar;51(3):296-301</RefSource>
<PMID Version="1">11891824</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2008 Oct;32(1):116-24</RefSource>
<PMID Version="1">18675914</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2009 Nov 4;29(44):13971-80</RefSource>
<PMID Version="1">19890007</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2012;7(1):e30834</RefSource>
<PMID Version="1">22303461</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Death Differ. 2011 Dec;18(12):1914-23</RefSource>
<PMID Version="1">21637291</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci Res. 2008 Jun;86(8):1711-20</RefSource>
<PMID Version="1">18214993</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 Nov 24;281(47):36303-16</RefSource>
<PMID Version="1">16963441</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2011 Feb;41(2):508-27</RefSource>
<PMID Version="1">21056667</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2005 Jul 15;382(3):309-11</RefSource>
<PMID Version="1">15925109</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Death Dis. 2012;3:e312</RefSource>
<PMID Version="1">22622131</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Parkinsons Dis. 2011;2011:789431</RefSource>
<PMID Version="1">21603187</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Mol Neurosci. 2013 Jan;49(1):105-15</RefSource>
<PMID Version="1">23065334</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2010 Mar;112(6):1593-604</RefSource>
<PMID Version="1">20067578</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Autophagy. 2008 Aug;4(6):770-82</RefSource>
<PMID Version="1">18594198</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Cell Sci. 2011 Apr 1;124(Pt 7):1115-25</RefSource>
<PMID Version="1">21385841</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Exp Cell Res. 2008 Jun 10;314(10):2055-65</RefSource>
<PMID Version="1">18445495</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2003 Jun 13;278(24):21542-9</RefSource>
<PMID Version="1">12679339</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2008 Jan 30;23(2):290-4</RefSource>
<PMID Version="1">17999435</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 2010 Nov 30;75(22):2017-20</RefSource>
<PMID Version="1">21115957</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurodegener Dis. 2012;10(1-4):238-41</RefSource>
<PMID Version="1">22204929</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2009 Sep;12(9):1129-35</RefSource>
<PMID Version="1">19684592</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Eur J Biochem. 2004 Jun;271(11):2060-6</RefSource>
<PMID Version="1">15153095</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2012 Sep 13;525(2):83-8</RefSource>
<PMID Version="1">22902902</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2009 May 15;284(20):13843-55</RefSource>
<PMID Version="1">19279012</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2006 Nov;60(5):557-69</RefSource>
<PMID Version="1">17120249</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Feb 15;21(4):890-9</RefSource>
<PMID Version="1">22080837</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nature. 2006 Jun 15;441(7095):885-9</RefSource>
<PMID Version="1">16625204</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Cell Proteomics. 2011 Jan;10(1):M110.001172</RefSource>
<PMID Version="1">20876399</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2009 Oct 15;18(20):3955-68</RefSource>
<PMID Version="1">19625296</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS Biol. 2010 Jan;8(1):e1000298</RefSource>
<PMID Version="1">20126261</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem J. 2007 Jul 15;405(2):307-17</RefSource>
<PMID Version="1">17447891</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2009 Dec 25;390(4):1229-34</RefSource>
<PMID Version="1">19878656</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 2007 Aug 1;43(3):372-83</RefSource>
<PMID Version="1">17602953</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Genes Dev. 2000 Aug 1;14(15):1837-51</RefSource>
<PMID Version="1">10921899</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2003 Jan;111(2):145-51</RefSource>
<PMID Version="1">12531866</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Stem Cell. 2013 Mar 7;12(3):354-67</RefSource>
<PMID Version="1">23472874</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2013 Feb 12;110(7):E602-10</RefSource>
<PMID Version="1">23324743</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2011 May 4;13(5):495-504</RefSource>
<PMID Version="1">21531332</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurochem Res. 2014;39(3):576-92</RefSource>
<PMID Version="1">23729298</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuron. 2004 Nov 18;44(4):601-7</RefSource>
<PMID Version="1">15541309</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurogenetics. 2008 May;9(2):83-94</RefSource>
<PMID Version="1">18097693</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2010 May;16(4):237-42</RefSource>
<PMID Version="1">19945904</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 1998 Oct 8;339(15):1044-53</RefSource>
<PMID Version="1">9761807</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2013 Jun 1;22(11):2129-40</RefSource>
<PMID Version="1">23396536</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2002 Dec;161(6):2087-98</RefSource>
<PMID Version="1">12466125</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuron. 2013 Feb 6;77(3):425-39</RefSource>
<PMID Version="1">23395371</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Pathol. 2004 Nov;204(4):438-49</RefSource>
<PMID Version="1">15495240</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Rev Neurosci. 2005 May;6(5):351-62</RefSource>
<PMID Version="1">15832199</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2012 Aug;18(7):819-23</RefSource>
<PMID Version="1">22525366</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2005 Jun;57(6):918-21</RefSource>
<PMID Version="1">15880653</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2006 Aug;23(2):329-41</RefSource>
<PMID Version="1">16750377</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nature. 2006 Jun 15;441(7095):880-4</RefSource>
<PMID Version="1">16625205</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neuropathol Exp Neurol. 2006 May;65(5):423-32</RefSource>
<PMID Version="1">16772866</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2006 Jan 15;15(2):223-32</RefSource>
<PMID Version="1">16321986</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2011;6(4):e18568</RefSource>
<PMID Version="1">21494637</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neuron. 2004 Nov 18;44(4):595-600</RefSource>
<PMID Version="1">15541308</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2010 Sep 29;30(39):13138-49</RefSource>
<PMID Version="1">20881132</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2013 Dec;1833(12):2900-10</RefSource>
<PMID Version="1">23916833</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 May 1;21(9):1931-44</RefSource>
<PMID Version="1">22228096</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D048049" MajorTopicYN="N">Extracellular Signal-Regulated MAP Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D060449" MajorTopicYN="N">Wnt Signaling Pathway</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">NIHMS540860</OtherID>
<OtherID Source="NLM">PMC4016799</OtherID>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autophagy</Keyword>
<Keyword MajorTopicYN="N">Cytoskeleton</Keyword>
<Keyword MajorTopicYN="N">LRRK2</Keyword>
<Keyword MajorTopicYN="N">MAPK</Keyword>
<Keyword MajorTopicYN="N">Mitophagy</Keyword>
<Keyword MajorTopicYN="N">Parkinson disease</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>07</Month>
<Day>31</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>10</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
<Month>11</Month>
<Day>03</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>11</Month>
<Day>15</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>11</Month>
<Day>15</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>9</Month>
<Day>4</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">24225420</ArticleId>
<ArticleId IdType="pii">S0925-4439(13)00330-X</ArticleId>
<ArticleId IdType="doi">10.1016/j.bbadis.2013.11.005</ArticleId>
<ArticleId IdType="pmc">PMC4016799</ArticleId>
<ArticleId IdType="mid">NIHMS540860</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Pennsylvanie</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Verma, Manish" sort="Verma, Manish" uniqKey="Verma M" first="Manish" last="Verma">Manish Verma</name>
</region>
<name sortKey="Chu, Charleen T" sort="Chu, Charleen T" uniqKey="Chu C" first="Charleen T" last="Chu">Charleen T. Chu</name>
<name sortKey="Steer, Erin K" sort="Steer, Erin K" uniqKey="Steer E" first="Erin K" last="Steer">Erin K. Steer</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Amérique/explor/PittsburghV1/Data/PubMed/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003135 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 003135 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Amérique
   |area=    PittsburghV1
   |flux=    PubMed
   |étape=   Checkpoint
   |type=    RBID
   |clé=     pubmed:24225420
   |texte=   ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i   -Sk "pubmed:24225420" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a PittsburghV1

This area was generated with Dilib version V0.6.38.
Data generation: Fri Jun 18 17:37:45 2021. Site generation: Fri Jun 18 18:15:47 2021

	Serveur d'exploration sur Pittsburgh
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur Pittsburgh

ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.

ERKed by LRRK2: a cell biological perspective on hereditary and sporadic Parkinson's disease.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki