Preparation of human cDNAs encoding expanded polyglutamine repeats

Matthew F. Peters, Christopher A. Ross

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


At least eight neurodegenerative diseases result from expansions of polyglutamine tracts encoded by CAG trinucleotide repeats. Although polyglutamine diseases typically have onset after age 50 in humans, these diseases can be modeled in animals and in cell culture by using highly expanded repeats to accelerate the pathogenesis. Unfortunately, current methods for preparing recombinant constructs with large glutamine tracts either alter the coding region adjacent to the repeat or yield highly unstable pure CAG repeats. We have developed a technique for expanding repeats that results in a more stable mix of CAG and CAA glutamine codons. We expect this technique to allow rapid preparation of highly expand repeats suitable for stable animal and cell culture models for any of the polyglutamine repeat diseases.

Original languageEnglish (US)
Pages (from-to)129-132
Number of pages4
JournalNeuroscience Letters
Issue number2
StatePublished - Nov 12 1999


  • CAG repeat
  • Huntington's disease
  • Polyglutamine
  • Trinulceotide repeat
  • Type IIS restriction enzyme

ASJC Scopus subject areas

  • General Neuroscience


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