Parkin: much more than a simple ubiquitin ligase.
Identifieur interne : 000911 ( PubMed/Corpus ); précédent : 000910; suivant : 000912Parkin: much more than a simple ubiquitin ligase.
Auteurs : C. Alves Da Costa ; F. CheclerSource :
- Neuro-degenerative diseases [ 1660-2862 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Brain (metabolism), Cell Death (genetics), Humans, Mice, Mutation (genetics), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Tumor Suppressor Protein p53 (genetics), Tumor Suppressor Protein p53 (metabolism), Ubiquitin-Protein Ligases (genetics), Ubiquitin-Protein Ligases (metabolism).
- MESH :
- chemical , genetics : Tumor Suppressor Protein p53, Ubiquitin-Protein Ligases.
- genetics : Cell Death, Mutation, Parkinson Disease.
- metabolism : Brain, Parkinson Disease, Tumor Suppressor Protein p53, Ubiquitin-Protein Ligases.
- pathology : Parkinson Disease.
- Animals, Humans, Mice.
Abstract
Parkin is mainly a cytosolic protein involved in a subset of Parkinson's disease (PD) cases referred to as autosomal juvenile recessive forms of PD. Most studies have established as a dogma that parkin function could be resumed as an ubiquitin ligase activity. Accordingly, several cellular functions ascribed to parkin derive from its ability to ubiquitinate a series of proteins, thereby rendering them prone to proteasomal degradation. Several lines of data indicated that parkin could display antiapoptotic properties and we demonstrated that indeed, parkin could downregulate the p53-dependent pathway. However, we showed that such function remained independent of parkin's ability to act as an ubiquitin ligase. Thus, we established that parkin repressed p53 transcription by physically interacting with its promoter. Here, we describe this novel parkin-associated transcription factor function and we speculate on putative additional transcriptional targets.
DOI: 10.1159/000332803
PubMed: 22204976
Links to Exploration step
pubmed:22204976Le document en format XML
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Checler</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:22204976</idno><idno type="pmid">22204976</idno><idno type="doi">10.1159/000332803</idno><idno type="wicri:Area/PubMed/Corpus">000911</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000911</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkin: much more than a simple ubiquitin ligase.</title><author><name sortKey="Alves Da Costa, C" sort="Alves Da Costa, C" uniqKey="Alves Da Costa C" first="C" last="Alves Da Costa">C. Alves Da Costa</name><affiliation><nlm:affiliation>Institut de Pharmacologie Moléculaire et Cellulaire et Institut de NeuroMédecine Moléculaire, Equipe Labellisée Fondation pour la Recherche Médicale, Sophia-Antipolis, Valbonne, France.</nlm:affiliation></affiliation></author><author><name sortKey="Checler, F" sort="Checler, F" uniqKey="Checler F" first="F" last="Checler">F. 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Here, we describe this novel parkin-associated transcription factor function and we speculate on putative additional transcriptional targets.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22204976</PMID><DateCreated><Year>2012</Year><Month>04</Month><Day>20</Day></DateCreated><DateCompleted><Year>2012</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1660-2862</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>1-4</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>Neuro-degenerative diseases</Title><ISOAbbreviation>Neurodegener Dis</ISOAbbreviation></Journal><ArticleTitle>Parkin: much more than a simple ubiquitin ligase.</ArticleTitle><Pagination><MedlinePgn>49-51</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1159/000332803</ELocationID><Abstract><AbstractText>Parkin is mainly a cytosolic protein involved in a subset of Parkinson's disease (PD) cases referred to as autosomal juvenile recessive forms of PD. Most studies have established as a dogma that parkin function could be resumed as an ubiquitin ligase activity. Accordingly, several cellular functions ascribed to parkin derive from its ability to ubiquitinate a series of proteins, thereby rendering them prone to proteasomal degradation. Several lines of data indicated that parkin could display antiapoptotic properties and we demonstrated that indeed, parkin could downregulate the p53-dependent pathway. However, we showed that such function remained independent of parkin's ability to act as an ubiquitin ligase. Thus, we established that parkin repressed p53 transcription by physically interacting with its promoter. Here, we describe this novel parkin-associated transcription factor function and we speculate on putative additional transcriptional targets.</AbstractText><CopyrightInformation>Copyright © 2011 S. Karger AG, Basel.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alves da Costa</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institut de Pharmacologie Moléculaire et Cellulaire et Institut de NeuroMédecine Moléculaire, Equipe Labellisée Fondation pour la Recherche Médicale, Sophia-Antipolis, Valbonne, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Checler</LastName><ForeName>F</ForeName><Initials>F</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>2011</Year><Month>12</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Neurodegener Dis</MedlineTA><NlmUniqueID>101189034</NlmUniqueID><ISSNLinking>1660-2854</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016159">Tumor Suppressor Protein p53</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><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</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="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016159" MajorTopicYN="N">Tumor Suppressor Protein p53</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">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>2011</Year><Month>06</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>09</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>12</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>12</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>8</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22204976</ArticleId><ArticleId IdType="pii">000332803</ArticleId><ArticleId IdType="doi">10.1159/000332803</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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