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dc.contributor.authorRunko, Alexander Peter
dc.contributor.authorGriswold, Anthony J.
dc.contributor.authorMin, Kyung-Tai
dc.date2022-08-11T08:08:51.000
dc.date.accessioned2022-08-23T16:10:16Z
dc.date.available2022-08-23T16:10:16Z
dc.date.issued2008-02-09
dc.date.submitted2009-02-23
dc.identifier.citationFEBS Lett. 2008 Mar 5;582(5):715-9. Epub 2008 Feb 5. <a href="http://dx.doi.org/10.1016/j.febslet.2008.01.046">Link to article on publisher's site</a>
dc.identifier.issn0014-5793 (Print)
dc.identifier.doi10.1016/j.febslet.2008.01.046
dc.identifier.pmid18258192
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32894
dc.description.abstractIn Friedreich's ataxia, reduction of the mitochondria protein frataxin results in the accumulation of iron and reactive oxygen species, which leads to oxidative damage, neurodegeneration and a diminished lifespan. Recent studies propose that frataxin might play a role in the antioxidative process. Here we show that overexpression of Drosophila frataxin in the mitochondria of female transgenic animals increases antioxidant capability, resistance to oxidative stress insults, and longevity. This suggests that Drosophila frataxin may function to protect the mitochondria from oxidative stresses and the ensuing cellular damage.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18258192&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.febslet.2008.01.046
dc.subjectAnimals; Animals, Genetically Modified; Antioxidants; Drosophila melanogaster; *Gene Expression; Gene Expression Regulation; Iron-Binding Proteins; *Longevity; Mitochondria; *Oxidative Stress; RNA, Messenger
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleOverexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila
dc.typeJournal Article
dc.source.journaltitleFEBS letters
dc.source.volume582
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1447
dc.identifier.contextkey733742
html.description.abstract<p>In Friedreich's ataxia, reduction of the mitochondria protein frataxin results in the accumulation of iron and reactive oxygen species, which leads to oxidative damage, neurodegeneration and a diminished lifespan. Recent studies propose that frataxin might play a role in the antioxidative process. Here we show that overexpression of Drosophila frataxin in the mitochondria of female transgenic animals increases antioxidant capability, resistance to oxidative stress insults, and longevity. This suggests that Drosophila frataxin may function to protect the mitochondria from oxidative stresses and the ensuing cellular damage.</p>
dc.identifier.submissionpathgsbs_sp/1447
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentPorter Neuroscience Research Center
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages715-9


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