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Epigenetic promoter silencing in Friedreich ataxia is dependent on repeat length

  • Published:2014-08-30 Issue:4 Volume:76 Page:522-528
  • ISSN:0364-5134
  • Container-title:Annals of Neurology
  • language:en
  • Short-container-title:Ann Neurol.

Author:

Chutake Yogesh K.1,Lam Christina1,Costello Whitney N.1,Anderson Michael2,Bidichandani Sanjay I.13

Affiliation:

1. Department of Pediatrics; University of Oklahoma College of Medicine; Oklahoma City OK

2. Department of Biostatistics and Epidemiology; University of Oklahoma College of Public Health; Oklahoma City OK

3. Department of Biochemistry and Molecular Biology; University of Oklahoma College of Medicine; Oklahoma City OK

Publisher

Wiley

Subject

Clinical Neurology,Neurology

Reference25 articles.

1. Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion;Campuzano;Science,1996

2. Clinical and genetic abnormalities in patients with Friedreich's ataxia;Durr;N Engl J Med,1996

3. The relationship between trinucleotide (GAA) repeat length and clinical features in Friedreich ataxia;Filla;Am J Hum Genet,1996

4. Phenotype correlation and intergenerational dynamics of the Friedreich ataxia GAA trinucleotide repeat;Monros;Am J Hum Genet,1997

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