huntington disease/arabidopsis

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Modeling human neurodegenerative diseases in transgenic systems.

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Transgenic systems are widely used to study the cellular and molecular basis of human neurodegenerative diseases. A wide variety of model organisms have been utilized, including bacteria (Escherichia coli), plants (Arabidopsis thaliana), nematodes (Caenorhabditis elegans), arthropods (Drosophila

A Polynucleotide Repeat Expansion Causing Temperature-Sensitivity Persists in Wild Irish Accessions of Arabidopsis thaliana.

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Triplet repeat expansions underlie several human genetic diseases such as Huntington's disease and Friedreich's ataxia. Although such mutations are primarily known from humans, a triplet expansion associated genetic defect has also been reported at the IIL1 locus in the Bur-0 accession of the model

The predominantly HEAT-like motif structure of huntingtin and its association and coincident nuclear entry with dorsal, an NF-kB/Rel/dorsal family transcription factor.

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BACKGROUND Huntington's disease (HD) pathogenesis is due to an expanded polyglutamine tract in huntingtin, but the specificity of neuronal loss compared with other polyglutamine disorders also implies a role for the protein's unknown inherent function. Huntingtin is moderately conserved, with 10

Repeat-encoded poly-Q tracts show statistical commonalities across species.

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BACKGROUND Among repetitive genomic sequence, the class of tri-nucleotide repeats has received much attention due to their association with human diseases. Tri-nucleotide repeat diseases are caused by excessive sequence length variability; diseases such as Huntington's disease and Fragile X syndrome

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