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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control</title><author><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Soubannier, Vincent" sort="Soubannier, Vincent" uniqKey="Soubannier V" first="Vincent" last="Soubannier">Vincent Soubannier</name><affiliation><nlm:aff id="au2"><institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Chen, Carol X" sort="Chen, Carol X" uniqKey="Chen C" first="Carol X" last="Chen">Carol X. Chen</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Mcbride, Heidi M" sort="Mcbride, Heidi M" uniqKey="Mcbride H" first="Heidi M" last="Mcbride">Heidi M. Mcbride</name><affiliation><nlm:aff id="au2"><institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24446486</idno><idno type="pmc">3989637</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3989637</idno><idno type="RBID">PMC:3989637</idno><idno type="doi">10.1002/embj.201385902</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000033</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000033</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control</title><author><name sortKey="Mclelland, Gian Luca" sort="Mclelland, Gian Luca" uniqKey="Mclelland G" first="Gian-Luca" last="Mclelland">Gian-Luca Mclelland</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Soubannier, Vincent" sort="Soubannier, Vincent" uniqKey="Soubannier V" first="Vincent" last="Soubannier">Vincent Soubannier</name><affiliation><nlm:aff id="au2"><institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Chen, Carol X" sort="Chen, Carol X" uniqKey="Chen C" first="Carol X" last="Chen">Carol X. Chen</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Mcbride, Heidi M" sort="Mcbride, Heidi M" uniqKey="Mcbride H" first="Heidi M" last="Mcbride">Heidi M. Mcbride</name><affiliation><nlm:aff id="au2"><institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author><author><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><affiliation><nlm:aff id="au1"><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></nlm:aff></affiliation></author></analytic><series><title level="j">The EMBO Journal</title><idno type="ISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). <italic>Parkin</italic> and <italic>PINK1</italic>, two genes associated with familial PD, have been implicated in the degradation of depolarized mitochondria via autophagy (mitophagy). Here, we describe the involvement of parkin and PINK1 in a vesicular pathway regulating mitochondrial quality control. This pathway is distinct from canonical mitophagy and is triggered by the generation of oxidative stress from within mitochondria. Wild-type but not PD-linked mutant parkin supports the biogenesis of a population of mitochondria-derived vesicles (MDVs), which bud off mitochondria and contain a specific repertoire of cargo proteins. These MDVs require PINK1 expression and ultimately target to lysosomes for degradation. We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">EMBO J</journal-id><journal-id journal-id-type="iso-abbrev">EMBO J</journal-id><journal-id journal-id-type="publisher-id">embj</journal-id><journal-title-group><journal-title>The EMBO Journal</journal-title></journal-title-group><issn pub-type="ppub">0261-4189</issn><issn pub-type="epub">1460-2075</issn><publisher><publisher-name>BlackWell Publishing Ltd</publisher-name><publisher-loc>Oxford, UK</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24446486</article-id><article-id pub-id-type="pmc">3989637</article-id><article-id pub-id-type="doi">10.1002/embj.201385902</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Parkin and PINK1 function in a vesicular trafficking pathway regulating mitochondrial quality control</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>McLelland</surname><given-names>Gian-Luca</given-names></name><xref ref-type="aff" rid="au1">1</xref></contrib><contrib contrib-type="author"><name><surname>Soubannier</surname><given-names>Vincent</given-names></name><xref ref-type="aff" rid="au2">2</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Carol X</given-names></name><xref ref-type="aff" rid="au1">1</xref></contrib><contrib contrib-type="author"><name><surname>McBride</surname><given-names>Heidi M</given-names></name><xref ref-type="aff" rid="au2">2</xref><xref ref-type="corresp" rid="cor2">**</xref></contrib><contrib contrib-type="author"><name><surname>Fon</surname><given-names>Edward A</given-names></name><xref ref-type="aff" rid="au1">1</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><aff id="au1"><label>1</label><institution>McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></aff><aff id="au2"><label>2</label><institution>Neuromuscular Group, Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University</institution><addr-line>Montreal, QC, Canada</addr-line></aff></contrib-group><author-notes><corresp id="cor1">* Corresponding author. Tel: +514 398 8398; Fax: +514 398 5214; E-mail: <email>ted.fon@mcgill.ca</email></corresp><corresp id="cor2">** Corresponding author. Tel: +514 398 1808; Fax: +514 398 1509; E-mail: <email>heidi.mcbride@mcgill.ca</email></corresp><fn><p><bold>Subject Categories</bold> Membrane & Intracellular Transport</p></fn></author-notes><pub-date pub-type="ppub"><day>18</day><month>2</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>20</day><month>1</month><year>2014</year></pub-date><volume>33</volume><issue>4</issue><fpage>282</fpage><lpage>295</lpage><history><date date-type="received"><day>05</day><month>6</month><year>2013</year></date><date date-type="rev-recd"><day>24</day><month>10</month><year>2013</year></date><date date-type="accepted"><day>05</day><month>12</month><year>2013</year></date></history><permissions><copyright-statement>© 2014 The Authors</copyright-statement><copyright-year>2014</copyright-year></permissions><related-article related-article-type="companion" id="d35e149" vol="33" page="277" xlink:href="24502976" ext-link-type="pubmed"></related-article><abstract><p>Mitochondrial dysfunction has long been associated with Parkinson's disease (PD). <italic>Parkin</italic> and <italic>PINK1</italic>, two genes associated with familial PD, have been implicated in the degradation of depolarized mitochondria via autophagy (mitophagy). Here, we describe the involvement of parkin and PINK1 in a vesicular pathway regulating mitochondrial quality control. This pathway is distinct from canonical mitophagy and is triggered by the generation of oxidative stress from within mitochondria. Wild-type but not PD-linked mutant parkin supports the biogenesis of a population of mitochondria-derived vesicles (MDVs), which bud off mitochondria and contain a specific repertoire of cargo proteins. These MDVs require PINK1 expression and ultimately target to lysosomes for degradation. We hypothesize that loss of this parkin- and PINK1-dependent trafficking mechanism impairs the ability of mitochondria to selectively degrade oxidized and damaged proteins leading, over time, to the mitochondrial dysfunction noted in PD.</p></abstract><kwd-group><kwd>MDV</kwd><kwd>mitochondria</kwd><kwd>mitophagy</kwd><kwd>Parkin</kwd><kwd>PINK1</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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