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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Programmed Cell Death in Parkinson's Disease</title><author><name sortKey="Venderova, Katerina" sort="Venderova, Katerina" uniqKey="Venderova K" first="Katerina" last="Venderova">Katerina Venderova</name><affiliation><nlm:aff id="af1">University of the Pacific, Thomas J. Long School of Pharmacy, Department of Physiology and Pharmacology, Stockton, California 95211</nlm:aff></affiliation></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S." last="Park">David S. Park</name><affiliation><nlm:aff id="af2">Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22908196</idno><idno type="pmc">3405826</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405826</idno><idno type="RBID">PMC:3405826</idno><idno type="doi">10.1101/cshperspect.a009365</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000B80</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B80</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Programmed Cell Death in Parkinson's Disease</title><author><name sortKey="Venderova, Katerina" sort="Venderova, Katerina" uniqKey="Venderova K" first="Katerina" last="Venderova">Katerina Venderova</name><affiliation><nlm:aff id="af1">University of the Pacific, Thomas J. Long School of Pharmacy, Department of Physiology and Pharmacology, Stockton, California 95211</nlm:aff></affiliation></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S." last="Park">David S. Park</name><affiliation><nlm:aff id="af2">Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada</nlm:aff></affiliation></author></analytic><series><title level="j">Cold Spring Harbor Perspectives in Medicine</title><idno type="eISSN">2157-1422</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Parkinson's disease is a debilitating disorder characterized by a progressive loss of dopaminergic neurons caused by programmed cell death. The aim of this review is to provide an up-to-date summary of the major programmed cell death pathways as they relate to PD. For a long time, programmed cell death has been synonymous with apoptosis but there now is evidence that other types of programmed cell death exist, such as autophagic cell death or programmed necrosis, and that these types of cell death are relevant to PD. The pathways and signals covered here include namely the death receptors, BCL-2 family, caspases, calpains, cdk5, p53, PARP-1, autophagy, mitophagy, mitochondrial fragmentation, and parthanatos. The review will present evidence from postmortem PD studies, toxin-induced models (especially MPTP/MPP+, 6-hydroxydopamine and rotenone), and from <italic>α-synuclein</italic>, <italic>LRRK2, Parkin, DJ-1</italic>, and <italic>PINK1</italic> genetic models of PD, both in vitro and in vivo.</p></div></front></TEI><pmc article-type="review-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">Cold Spring Harb Perspect Med</journal-id><journal-id journal-id-type="iso-abbrev">Cold Spring Harb Perspect Med</journal-id><journal-id journal-id-type="publisher-id">cshperspectmed</journal-id><journal-id journal-id-type="hwp">cshperspectmed</journal-id><journal-title-group><journal-title>Cold Spring Harbor Perspectives in Medicine</journal-title></journal-title-group><issn pub-type="epub">2157-1422</issn><publisher><publisher-name>Cold Spring Harbor Laboratory Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22908196</article-id><article-id pub-id-type="pmc">3405826</article-id><article-id pub-id-type="doi">10.1101/cshperspect.a009365</article-id><article-id pub-id-type="publisher-id">a009365</article-id><article-categories><subj-group subj-group-type="hwp-journal-coll"><subject>071</subject></subj-group><subj-group subj-group-type="heading"><subject>Perspectives</subject></subj-group></article-categories><title-group><article-title>Programmed Cell Death in Parkinson's Disease</article-title><alt-title alt-title-type="left-running">K. Venderova and D.S. Park</alt-title><alt-title alt-title-type="right-running">Programmed Cell Death in PD</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Venderova</surname><given-names>Katerina</given-names></name><xref ref-type="aff" rid="af1">1</xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>David S.</given-names></name><xref ref-type="aff" rid="af2">2</xref></contrib></contrib-group><aff id="af1"><label>1</label>University of the Pacific, Thomas J. Long School of Pharmacy, Department of Physiology and Pharmacology, Stockton, California 95211</aff><aff id="af2"><label>2</label>Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada</aff><author-notes><corresp><italic>Correspondence:</italic><email>kvenderova@pacific.edu</email></corresp></author-notes><pub-date pub-type="ppub"><month>8</month><year>2012</year></pub-date><volume>2</volume><issue>8</issue><elocation-id>a009365</elocation-id><permissions><copyright-statement>Copyright © 2012 Cold Spring Harbor Laboratory Press; all rights reserved</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="cshperspectmed-PKD-a009365.pdf"></self-uri><abstract><p>Parkinson's disease is a debilitating disorder characterized by a progressive loss of dopaminergic neurons caused by programmed cell death. The aim of this review is to provide an up-to-date summary of the major programmed cell death pathways as they relate to PD. For a long time, programmed cell death has been synonymous with apoptosis but there now is evidence that other types of programmed cell death exist, such as autophagic cell death or programmed necrosis, and that these types of cell death are relevant to PD. The pathways and signals covered here include namely the death receptors, BCL-2 family, caspases, calpains, cdk5, p53, PARP-1, autophagy, mitophagy, mitochondrial fragmentation, and parthanatos. The review will present evidence from postmortem PD studies, toxin-induced models (especially MPTP/MPP+, 6-hydroxydopamine and rotenone), and from <italic>α-synuclein</italic>, <italic>LRRK2, Parkin, DJ-1</italic>, and <italic>PINK1</italic> genetic models of PD, both in vitro and in vivo.</p></abstract><abstract abstract-type="precis"><p>Parkinson's disease involves apoptosis, autophagic cell death, and programmed necrosis. The contribution of each depends on the stimulus or stressor, its concentration and timing, and brain region or cell type.</p></abstract><counts><page-count count="23"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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