SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat
- 1 September 1995
- Vol. 82 (6) , 937-948
- https://doi.org/10.1016/0092-8674(95)90273-2
Abstract
No abstract availableKeywords
This publication has 29 references indexed in Scilit:
- Gametic and somatic tissue–specific heterogeneity of the expanded SCA1 CAG repeat in spinocerebellar ataxia type 1Nature Genetics, 1995
- In Vivo Viability of Postmitotic Purkinje Neurons Requires pRb Family Member FunctionMolecular and Cellular Neuroscience, 1995
- Stability of an expanded trinucleotide repeat in the androgen receptor gene in transgenic miceNature Genetics, 1995
- The Haw River Syndrome: Dentatorubropallidoluysian atrophy (DRPLA) in an African–American familyNature Genetics, 1994
- Mapping and cloning of the critical region for the spinocerebellar ataxia type 1 gene (SCA1) in a yeast artificial chromosome contig spanning 1.2 MbGenomics, 1993
- Presymptomatic analysis of spinocerebellar ataxia type 1 (SCA1) via the expansion of the SCA1 CAG-repeat in a large pedigree displaying anticipation and parental male biasHuman Molecular Genetics, 1993
- A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomesCell, 1993
- Disrupted cerebellar cortical development and progressive degeneration of Purkinje cells in SV40 T antigen transgenic miceNeuron, 1992
- Spinocerebellar ataxia: Variable age of onset and linkage to human leukocyte antigen in a large kindredAnnals of Neurology, 1988
- Homozygotes for Huntington's diseaseNature, 1987