Linked Life Data

18258192

Source:http://linkedlifedata.com/resource/pubmed/id/18258192

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-2-26
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
582
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
715-9
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Overexpression of frataxin in the mitochondria increases resistance to oxidative stress and extends lifespan in Drosophila.
pubmed:affiliation
Porter Neuroscience Research Center, MSC 3705, NINDS, NIH, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural