Transgenic mouse models of neurodegenerative disease caused by CAG/polyglutamine expansions
- 1 November 1997
- journal article
- review article
- Published by Elsevier in Molecular Medicine Today
- Vol. 3 (11) , 508-515
- https://doi.org/10.1016/s1357-4310(97)01142-8
Abstract
No abstract availableKeywords
This publication has 41 references indexed in Scilit:
- Transgenic models of Huntington's diseaseHuman Molecular Genetics, 1997
- Polyglutamine expansion as a pathological epitope in Huntington's disease and four dominant cerebellar ataxiasNature, 1995
- Increased apoptosis and early embryonic lethality in mice nullizygous for the Huntington's disease gene homologueNature Genetics, 1995
- When more is less: Pathogenesis of glutamine repeat neurodegenerative diseasesNeuron, 1995
- Inactivation of the Mouse Huntington's Disease Gene Homolog HdhScience, 1995
- Targeted disruption of the Huntington's disease gene results in embryonic lethality and behavioral and morphological changes in heterozygotesCell, 1995
- Expression analysis of the ataxin–1 protein in tissues from normal and spinocerebellar ataxia type 1 individualsNature Genetics, 1995
- Abnormal gene product identified in hereditary dentatorubral–pallidoluysian atrophy (DRPLA) brainNature Genetics, 1995
- Cellular localization of the Huntington's disease protein and discrimination of the normal and mutated formNature Genetics, 1995
- Evidence from antibody studies that the CAG repeat in the Huntington disease gene is expressed in the proteinHuman Molecular Genetics, 1995