dc.contributor.author |
Vives-Bauzà, Cristòfol |
|
dc.contributor.author |
Przedborki, Serge |
|
dc.date.accessioned |
2018-10-08T10:33:41Z |
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dc.identifier.uri |
http://hdl.handle.net/11201/147981 |
|
dc.description.abstract |
For decades, it has been presumed that mitochondrial dysfunction, in the form of impaired complex I activity, may contribute to the cause of Parkinson disease (PD). ( 1) The discovery that several gene mutations cause familial forms of PD ( 1) has led to a renewed enthusiasm for the mitochondrial hypothesis of PD, but this time from a quite distinct and, perhaps, more realistic angle. Among these genes, those that code for PTEN-induced kinase-1 (PINK1) ( 2) and for the E3-ubiquitin ligase Parkin ( 3) did attract major interest from mitochondriologists, in part, because both proteins interact with each other and apparently function, genetically, within the same molecular pathway to modulate mitochondrial dynamics in Drosophila. ( 4-6). |
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dc.format |
application/pdf |
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dc.relation.isformatof |
Versió postprint del document publicat a: https://doi.org/10.4161/auto.6.5.12068 |
|
dc.relation.ispartof |
Autophagy, 2010, vol. 6, num. 5, p. 674-675 |
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dc.subject.classification |
616.8 - Neurologia. Neuropatologia. Sistema nerviós |
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dc.subject.other |
616.8 - Neurology. Neuropathology. Nervous system |
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dc.title |
PINK1 points Parkin to mitochondria |
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dc.type |
info:eu-repo/semantics/article |
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dc.type |
info:eu-repo/semantics/acceptedVersion |
|
dc.date.updated |
2018-10-08T10:33:42Z |
|
dc.date.embargoEndDate |
info:eu-repo/date/embargoEnd/2075-01-01 |
|
dc.embargo |
2075-01-01 |
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dc.rights.accessRights |
info:eu-repo/semantics/embargoedAccess |
|
dc.identifier.doi |
https://doi.org/10.4161/auto.6.5.12068 |
|