PINK1 points Parkin to mitochondria

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dc.contributor.author Vives-Bauzà, Cristòfol
dc.contributor.author Przedborki, Serge
dc.date.accessioned 2018-10-08T10:33:41Z
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).
dc.format application/pdf
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
dc.subject.classification 616.8 - Neurologia. Neuropatologia. Sistema nerviós
dc.subject.other 616.8 - Neurology. Neuropathology. Nervous system
dc.title PINK1 points Parkin to mitochondria
dc.type info:eu-repo/semantics/article
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
dc.rights.accessRights info:eu-repo/semantics/embargoedAccess
dc.identifier.doi https://doi.org/10.4161/auto.6.5.12068


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