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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2002-6-13
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pubmed:abstractText |
In the search for neuroprotective factors in Huntington's disease, we found that insulin growth factor 1 via activation of the serine/threonine kinase Akt/PKB is able to inhibit neuronal death specifically induced by mutant huntingtin containing an expanded polyglutamine stretch. The IGF-1/Akt pathway has a dual effect on huntingtin-induced toxicity, since activation of this pathway also results in a decrease in the formation of intranuclear inclusions of mutant huntingtin. We demonstrate that huntingtin is a substrate of Akt and that phosphorylation of huntingtin by Akt is crucial to mediate the neuroprotective effects of IGF-1. Finally, we show that Akt is altered in Huntington's disease patients. Taken together, these results support a potential role of the Akt pathway in Huntington's disease.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/AKT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/HD protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1534-5807
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
831-7
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12062094-Cell Death,
pubmed-meshheading:12062094-Cells, Cultured,
pubmed-meshheading:12062094-Corpus Striatum,
pubmed-meshheading:12062094-Enzyme Activation,
pubmed-meshheading:12062094-Humans,
pubmed-meshheading:12062094-Huntington Disease,
pubmed-meshheading:12062094-Inclusion Bodies,
pubmed-meshheading:12062094-Insulin-Like Growth Factor I,
pubmed-meshheading:12062094-Nerve Tissue Proteins,
pubmed-meshheading:12062094-Neurons,
pubmed-meshheading:12062094-Nuclear Proteins,
pubmed-meshheading:12062094-Phosphorylation,
pubmed-meshheading:12062094-Point Mutation,
pubmed-meshheading:12062094-Protein-Serine-Threonine Kinases,
pubmed-meshheading:12062094-Proto-Oncogene Proteins,
pubmed-meshheading:12062094-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:12062094-Recombinant Fusion Proteins,
pubmed-meshheading:12062094-Substrate Specificity
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pubmed:year |
2002
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pubmed:articleTitle |
The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves Huntingtin phosphorylation by Akt.
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pubmed:affiliation |
UMR 146 CNRS/Institut Curie, Centre Universitaire, 91405 Orsay Cedex, France.
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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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