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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2004-3-15
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pubmed:abstractText |
Ataxia-telangiectasia is caused by mutations in the ATM gene, the protein product of which is essential for effective response to double-stranded DNA breaks. Loss of ATM function explains most aspects of the disease, but not the cerebellar neurodegeneration characteristic of the disease. Mice lacking ATM provide an excellent model of the human disorder. In addition to deficient response to DNA damage, these mice exhibit oxidative stress, which we hypothesized is the cause of cerebellar dysfunction. We show that treatment with a catalytic antioxidant corrects the neurobehavioral deficit in these mice.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0891-5849
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
36
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
938-42
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:15019978-Animals,
pubmed-meshheading:15019978-Antioxidants,
pubmed-meshheading:15019978-Ataxia Telangiectasia,
pubmed-meshheading:15019978-Brain,
pubmed-meshheading:15019978-Catalysis,
pubmed-meshheading:15019978-Cell Cycle Proteins,
pubmed-meshheading:15019978-DNA-Binding Proteins,
pubmed-meshheading:15019978-Disease Models, Animal,
pubmed-meshheading:15019978-Fatty Acids,
pubmed-meshheading:15019978-Mice,
pubmed-meshheading:15019978-Mice, Knockout,
pubmed-meshheading:15019978-Organometallic Compounds,
pubmed-meshheading:15019978-Oxidation-Reduction,
pubmed-meshheading:15019978-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15019978-Rotarod Performance Test,
pubmed-meshheading:15019978-Salicylates,
pubmed-meshheading:15019978-Tumor Suppressor Proteins
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pubmed:year |
2004
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pubmed:articleTitle |
Treatment with a catalytic antioxidant corrects the neurobehavioral defect in ataxia-telangiectasia mice.
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pubmed:affiliation |
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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