Linked Life Data

19699304

Source:http://linkedlifedata.com/resource/pubmed/id/19699304

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pubmed-article:19699304pubmed:dateCreated2009-10-12lld:pubmed
pubmed-article:19699304pubmed:abstractTextThe Huntington's disease (HD) mutation causes polyglutamine expansion in huntingtin (Htt) and neurodegeneration. Htt interacts with a complex containing Rab11GDP and is involved in activation of Rab11, which functions in endosomal recycling and neurite growth and long-term potentiation. Like other Rab proteins, Rab11GDP undergoes nucleotide exchange to Rab11GTP for its activation. Here we show that striatal membranes of HD(140Q/140Q) knock-in mice are impaired in supporting conversion of Rab11GDP to Rab11GTP. Dominant negative Rab11 expressed in the striatum and cortex of normal mice caused neuropathology and motor dysfunction, suggesting that a deficiency in Rab11 activity is pathogenic in vivo. Primary cortical neurons from HD(140Q/140Q) mice were delayed in recycling transferrin receptors back to the plasma membrane. Partial rescue from glutamate-induced cell death occurred in HD neurons expressing dominant active Rab11. We propose a novel mechanism of HD pathogenesis arising from diminished Rab11 activity at recycling endosomes.lld:pubmed
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pubmed-article:19699304pubmed:authorpubmed-author:KegelKimberly...lld:pubmed
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pubmed-article:19699304pubmed:authorpubmed-author:EstevesMiguel...lld:pubmed
pubmed-article:19699304pubmed:issnTypeElectroniclld:pubmed
pubmed-article:19699304pubmed:volume36lld:pubmed
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pubmed-article:19699304pubmed:pagination374-83lld:pubmed
pubmed-article:19699304pubmed:dateRevised2010-12-3lld:pubmed
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pubmed-article:19699304pubmed:year2009lld:pubmed
pubmed-article:19699304pubmed:articleTitleDisruption of Rab11 activity in a knock-in mouse model of Huntington's disease.lld:pubmed
pubmed-article:19699304pubmed:affiliationDepartment of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA. xli12@partners.orglld:pubmed
pubmed-article:19699304pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19699304pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:19699304pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:19699304pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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