Ectopically Expressed CAG Repeats Cause Intranuclear Inclusions and a Progressive Late Onset Neurological Phenotype in the Mouse
Open Access
- 1 December 1997
- Vol. 91 (6) , 753-763
- https://doi.org/10.1016/s0092-8674(00)80464-x
Abstract
No abstract availableKeywords
This publication has 27 references indexed in Scilit:
- Monoamine deficiency in a transgenic (Hprt−) mouse model of Lesch-Nyhan syndromePublished by Elsevier ,2003
- Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in BrainScience, 1997
- Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the α1A-voltage-dependent calcium channelNature Genetics, 1997
- Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic MiceCell, 1996
- The expanding world of ataxinsNature Genetics, 1996
- Monoclonal Antibodies Directed against the Amino-Terminal Domain of Human TBP Cross-React with TBP from Other SpeciesHybridoma, 1996
- Trinucleotide repeats in neurologic diseases: An hypothesis concerning the pathogenesis of Huntington's disease, Kennedy's disease, and spinocerebellar ataxia type ILife Sciences, 1994
- Derivation of completely cell culture-derived mice from early-passage embryonic stem cells.Proceedings of the National Academy of Sciences, 1993
- Mouse models of hypoxanthine phosphoribosyltransferase deficiencyJournal of Inherited Metabolic Disease, 1992
- Amphetamine-induced behavioral phenotype in a hypoxanthine-guanine phosphoribosyltransferase-deficient mouse model of Lesch-Nyhan syndrome.Behavioral Neuroscience, 1991