MartinJBPathogenesis of neurodegenerative disorders: The role of dynamic mutations. Neuroreport1996; 8: i–vii.
2.
BinghamPMScottMOWangS, et al. Stability of an expanded trinucleotide repeat in the androgen receptor gene in transgenic mice. Nat Genet1995; 9:191–196.
3.
ReddySSmithDBJRichMM, et al. Mice lacking the myotonic dystrophy protein kinase develop a late onset progressive myopathy. Nat Genet1996; 13:325–335.
4.
JansenGGroenenPJTABachnerD, et al. Abnormal myotonic dystrophy protein kinase levels produce only mild myopathy in mice. Nat Genet1996; 13:316–323.
5.
GourdonGRadvanyiFLiaA-S, et al. Moderate intergenerational and somatic instability of a 55-CTG repeat in transgenic mice. Nat Genet1997; 15:190–192.
DuyaoMPAuerbachABRyanA, et al. Inactivation of the mouse Huntington's disease gene homolog HdhScience1995; 269:407–410.
8.
NasirJFlorescoSBO'KuskyJR, et al. Targeted disruption of the Huntington's disease gene results in embryonic lethality and behavioral and morphological changes in heterozygotes. Cell1995; 81:811–823.
9.
GoldbergYPKalchmanMAMetzlerM, et al. Absence of disease phenotype and intergenerational stability of the CAG repeat in transgenic mice expressing the human Huntington's disease transcript. Hum Mol Genet1996; 5:177–185.
10.
MangiariniLSathasivamKSellerM, et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell1996; 87:493–506.
11.
MangiariniLSathasivamKMahalAMottRSellerMBatesG.Instability of highly expanded CAG repeats in mice transgenic for the Huntington's disease mutation. Nat Genet1997; 15:197–200.
12.
BurrightENClarkHBServadioA, et al. SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat. Cell1995; 82:937–948.
13.
IkedaHYamaguchiMSugaiSAzeYNarumiyaSKakizukaA.Expanded polyglutamine in the Machado-Joseph disease protein induced cell death in vitro and in vivo. Nat Genet1996; 13:196–202.
14.
AlmqvistESpenceNNicholK, et al. Ancestral differences in the distribution of the A2642 glutamic acid polymorphism are associated with varying CAG repeat lengths on normal chromosomes: Insights into the genetic evolution of Huntington's disease. Hum Mol Genet1995; 4:207–214.
15.
ChungM-YRanumLPWDuvickLAServadioAZoghbiHYOrrHTEvidence for a mechanism predisposing to intergenerational CAG repeat instability in spinocerebellar ataxia type 1. Nat Genet1993; 5:254–258.
16.
NevilleCEMahadevanMSBarceloJMKornelukRGHigh resolution genetic analysis suggests one ancestral predisposing haplotype for the origin of the myotonic dystrophy mutation. Hum Mol Genet1994; 3:45–51.
17.
The Huntington's Disease Collaborative Research Group. a novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. Cell1993; 72:971–983.
IshitaniRChuangDMGlyceraldehyde-3-phosphate dehydrogenase antisense oligodeoxynucleotides protect against cytosine arabinonucleoside-induced apoptosis in cultured cerebellar neurons. Proc Natl Acad Sci U S A1996; 93:9937–9941.
20.
GoldbergYPNicholsonDWRasperDM, et al. Cleavage of huntíngtín by apopain, a proapoptotic cysteine protease, is modulated by the polyglutamine tract. Nat Genet1996; 13:442–449.
21.
ZoghbiHYThe expanding world of ataxins. Nat Genet1996; 14:237–238.
22.
HamshereMGBrookJDMyotonic dystrophy, knockouts, warts and all. Trends Genet1996; 12:332–334.
23.
BoucherCAKingSKCareyN, et al. A novel homeodomain-encoding gene is associated with a large CpG island interrupted by the myotonic dystrophy unstable (CTG)n repeat. Hum Mol Genet1995; 4:1919–1925.
24.
TimchenkoLTMillerJWTimchenkoNA, et al. Identification of a (CUG)n triplet repeat RNA-binding protein and its expression in myotonic dystrophy. Nucleic Acids Res1996; 24:4407–4414.
