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Rhes deletion is neuroprotective in the 3-nitropropionic acid model of Huntington's disease

Academic Article
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Overview

authors

  • Mealer, R. G.
  • Subramaniam, Srinivasa
  • Snyder, S. H.

publication date

  • February 2013

journal

  • Journal of Neuroscience  Journal

abstract

  • Although the mutated protein causing Huntington's disease (HD) is expressed throughout the body, the major pathology of HD is localized to the striatum of the brain. We previously reported that the striatal-enriched protein Rhes binds the mutated huntingtin protein and enhances its cytotoxicity. We now demonstrate that Rhes-deleted mice are dramatically protected from neurotoxicity and motor dysfunction in a striatal-specific model of HD elicited by 3-nitropropionic acid. This finding suggests that Rhes may, in part, determine the striatal selectivity of HD.

subject areas

  • Animals
  • Disease Models, Animal
  • Exploratory Behavior
  • GTP-Binding Proteins
  • Huntington Disease
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neurotoxins
  • Nitro Compounds
  • Propionates
  • Psychomotor Performance
  • Succinate Dehydrogenase
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Identity

PubMed Central ID

  • PMC3667505

International Standard Serial Number (ISSN)

  • 0270-6474

Digital Object Identifier (DOI)

  • 10.1523/jneurosci.3730-12.2013

PubMed ID

  • 23447628
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Additional Document Info

start page

  • 4206

end page

  • 4210

volume

  • 33

issue

  • 9

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