Disruption of Axonal Transport by Loss of Huntingtin or Expression of Pathogenic PolyQ Proteins in Drosophila

We tested whether proteins implicated in Huntington's and other polyglutamine (polyQ) expansion diseases can cause axonal transport defects. Reduction of Drosophila huntingtin and expression of proteins containing pathogenic polyQ repeats disrupt axonal transport. Pathogenic polyQ proteins accu...

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Veröffentlicht in:	Neuron (Cambridge, Mass.) Mass.), 2003-09, Vol.40 (1), p.25-40
Hauptverfasser:	Gunawardena, Shermali, Her, Lu-Shiun, Brusch, Richard G., Laymon, Robert A., Niesman, Ingrid R., Gordesky-Gold, Beth, Sintasath, Louis, Bonini, Nancy M., Goldstein, Lawrence S.B.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Animals, Genetically Modified Apoptosis Axonal Transport - physiology Cell Death - physiology Cytoskeleton Defects Disease Drosophila Drosophila Proteins - biosynthesis Drosophila Proteins - deficiency Drosophila Proteins - genetics Female Gene Expression Regulation - physiology Genes Genotype & phenotype Humans Huntingtin Protein Huntington Disease - genetics Huntington Disease - metabolism Huntington Disease - pathology Insects Male Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - deficiency Nerve Tissue Proteins - genetics Neurodegeneration Neurons Nuclear Proteins - biosynthesis Nuclear Proteins - deficiency Nuclear Proteins - genetics Peptides - deficiency Peptides - genetics Peptides - metabolism Phenotype Proteins Rodents
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