Parkinson's disease: to live or die by autophagy.
Identifieur interne : 001D99 ( Main/Exploration ); précédent : 001D98; suivant : 001E00Parkinson's disease: to live or die by autophagy.
Auteurs : Isabella Irrcher [Canada] ; David S. ParkSource :
- Science signaling [ 1937-9145 ] ; 2009.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Apoptosis Regulatory Proteins.
- etiology : Parkinson Disease.
- metabolism : Neurons, Parkinson Disease.
- physiology : Autophagy, Cell Survival, Signal Transduction.
- Humans, Models, Biological.
Abstract
The identification of the molecular mechanisms underlying neuronal survival continues to be the subject of intensive research efforts as the incidence of age-related neurodegenerative diseases rises. Amid a complex mélange of environmental and genetic factors that contribute to disease manifestation, much effort has been dedicated to understanding the underlying signaling mechanisms that regulate neuronal survival. A recent study by Yang et al. sheds new light on an intracellular quality-control system that regulates the constitutive abundance of a neuronal survival factor through chaperone-mediated autophagy and links the deregulation of this pathway to Parkinson's disease. Although the primary function of autophagy in most cell types has commonly been thought to be an adaptive response to starvation, it has been proposed that proper functioning of this system is essential for neuronal survival and that its deregulation leads to neurodegeneration.
DOI: 10.1126/scisignal.265pe21
PubMed: 19351953
Affiliations:
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Le document en format XML
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Park</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19351953</idno><idno type="pmid">19351953</idno><idno type="doi">10.1126/scisignal.265pe21</idno><idno type="wicri:Area/PubMed/Corpus">000E84</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000E84</idno><idno type="wicri:Area/PubMed/Curation">000E84</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000E84</idno><idno type="wicri:Area/PubMed/Checkpoint">000E84</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000E84</idno><idno type="wicri:Area/Ncbi/Merge">000A58</idno><idno type="wicri:Area/Ncbi/Curation">000A58</idno><idno type="wicri:Area/Ncbi/Checkpoint">000A58</idno><idno type="wicri:Area/Main/Merge">001F47</idno><idno type="wicri:Area/Main/Curation">001D99</idno><idno type="wicri:Area/Main/Exploration">001D99</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkinson's disease: to live or die by autophagy.</title><author><name sortKey="Irrcher, Isabella" sort="Irrcher, Isabella" uniqKey="Irrcher I" first="Isabella" last="Irrcher">Isabella Irrcher</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. Park</name></author></analytic><series><title level="j">Science signaling</title><idno type="eISSN">1937-9145</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Autophagy (physiology)</term><term>Cell Survival (physiology)</term><term>Humans</term><term>Models, Biological</term><term>Neurons (metabolism)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (metabolism)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apoptosis Regulatory Proteins</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Cell Survival</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Models, Biological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The identification of the molecular mechanisms underlying neuronal survival continues to be the subject of intensive research efforts as the incidence of age-related neurodegenerative diseases rises. Amid a complex mélange of environmental and genetic factors that contribute to disease manifestation, much effort has been dedicated to understanding the underlying signaling mechanisms that regulate neuronal survival. A recent study by Yang et al. sheds new light on an intracellular quality-control system that regulates the constitutive abundance of a neuronal survival factor through chaperone-mediated autophagy and links the deregulation of this pathway to Parkinson's disease. Although the primary function of autophagy in most cell types has commonly been thought to be an adaptive response to starvation, it has been proposed that proper functioning of this system is essential for neuronal survival and that its deregulation leads to neurodegeneration.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. Park</name></noCountry><country name="Canada"><noRegion><name sortKey="Irrcher, Isabella" sort="Irrcher, Isabella" uniqKey="Irrcher I" first="Isabella" last="Irrcher">Isabella Irrcher</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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