Capucin does not modify the toxicity of a mutant Huntingtin fragment in vivo

Neurobiol Aging. 2012 Aug;33(8):1845.e5-6. doi: 10.1016/j.neurobiolaging.2012.01.009. Epub 2012 Feb 24.

Abstract

Genes selectively expressed in the striatum may be involved in the preferential vulnerability of striatal neurons to Huntington's disease (HD). Here, we investigated whether perturbations of Capucin expression, which is enriched in the striatum and downregulated in Huntington's disease models, could modify the neurotoxicity induced by the injection of a lentiviral vector encoding a short N-terminal fragment of mutant Huntingtin (mHtt) into the mouse striatum. Neither constitutive Capucin deficiency in knockout mice nor lentiviral vector-mediated Capucin overexpression in the striatum of adult wild type mice significantly modified vulnerability to the mHtt fragment in vivo, suggesting that Capucin has no impact on mHtt toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Corpus Striatum / metabolism*
  • Corpus Striatum / pathology*
  • Huntingtin Protein
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Knockout
  • Mutation
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism*
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism*

Substances

  • Htt protein, mouse
  • Huntingtin Protein
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Syndig1l protein, mouse