Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease.
Identifieur interne : 000680 ( PubMed/Checkpoint ); précédent : 000679; suivant : 000681Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease.
Auteurs : Olga Corti [France] ; Alexis BriceSource :
- Current opinion in neurobiology [ 1873-6882 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Humans, Mitochondria (genetics), Mitochondria (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Protein Kinases (genetics), Protein Kinases (metabolism), Ubiquitin-Protein Ligases (genetics), Ubiquitin-Protein Ligases (metabolism).
- MESH :
- chemical , genetics : Protein Kinases, Ubiquitin-Protein Ligases.
- genetics : Mitochondria, Parkinson Disease.
- metabolism : Mitochondria, Parkinson Disease, Protein Kinases, Ubiquitin-Protein Ligases.
- physiopathology : Parkinson Disease.
- Animals, Humans.
Abstract
Mitochondrial dysfunction has long been suspected to play a key role in neurodegeneration in Parkinson's disease. PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.
DOI: 10.1016/j.conb.2012.11.002
PubMed: 23206589
Affiliations:
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pubmed:23206589Le document en format XML
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PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23206589</PMID><DateCreated><Year>2013</Year><Month>01</Month><Day>29</Day></DateCreated><DateCompleted><Year>2013</Year><Month>07</Month><Day>24</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-6882</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Current opinion in neurobiology</Title><ISOAbbreviation>Curr. Opin. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>Mitochondrial quality control turns out to be the principal suspect in parkin and PINK1-related autosomal recessive Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>100-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.conb.2012.11.002</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0959-4388(12)00164-X</ELocationID><Abstract><AbstractText>Mitochondrial dysfunction has long been suspected to play a key role in neurodegeneration in Parkinson's disease. PINK1 and Parkin, the products of two genes responsible for autosomal recessive Parkinsonian syndromes with early onset, act as a quality control system on the outer mitochondrial membrane to preserve mitochondrial integrity. While doing so, they interact with multiple molecular actors in processes regulating mitochondrial biology and cell survival. The physiological conditions that mobilize these processes in neurons, and the mechanisms underlying their integration and spatiotemporal coordination, remain to be elucidated. Understanding how dysfunction of these house-keeping pathways leads to the preferential degeneration of a specific neuronal population in Parkinson's disease is a major challenge for future research.</AbstractText><CopyrightInformation>Copyright © 2012 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>Alexis</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Curr Opin Neurobiol</MedlineTA><NlmUniqueID>9111376</NlmUniqueID><ISSNLinking>0959-4388</ISSNLinking></MedlineJournalInfo><ChemicalList><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><Chemical><RegistryNumber>EC 2.7.-</RegistryNumber><NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C433927">PTEN-induced putative kinase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044767" MajorTopicYN="N">Ubiquitin-Protein Ligases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>10</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>11</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>11</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>12</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>7</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23206589</ArticleId><ArticleId IdType="pii">S0959-4388(12)00164-X</ArticleId><ArticleId IdType="doi">10.1016/j.conb.2012.11.002</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><noCountry><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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