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A gene, ATM, that is mutated in the autosomal recessive disorder ataxia telangiectasia (AT) was identified by positional cloning on chromosome 11q22-23. AT is characterized by cerebellar degeneration, immunodeficiency, chromosomal instability, cancer predisposition, radiation sensitivity, and cell cycle abnormalities. The disease is genetically(More)
The morphological picture of primate phylogeny has not unambiguously identified the nearest outgroup of Anthropoidea and has not resolved the branching pattern within Hominoidea. The molecular picture provides more resolution and clarifies the systematics of Hominoidea. Protein and DNA evidence divides Hominoidea into Hylobatidae (gibbons) and Hominidae,(More)
We have used RNA in situ hybridization to study the regional expression of the Huntington's disease gene (HD) and its rat homologue in brain and selected nonneural tissues. The HD transcript was expressed throughout the brain in both rat and human, especially in the neurons of the dentate gyrus and pyramidal neurons of the hippocampal formation, cerebellar(More)
Phylogenetic analysis of extensive nucleotide sequence data from primate beta-globin gene clusters elucidates the systematics and evolution of the order Primates and reveals that rates of accumulation of mutations vary by as much as a factor of seven among different primate lineages. The picture of primate phylogeny from DNA sequences clarifies many(More)
1986. AND M. B. CALFORD. Somatosensory cortical representation in the Australian ghost bat, Macroderma gigas. 1987. Amino acid sequence versus morphological data and the interordinal relations of mammals. Did powered flight evolve once or twice in mammals? A heated debate has recently developed concerning the phylogenetic relationships of Microchiroptera,(More)
In 1993, the genetic abnormality responsible for Huntington's disease was identified as a trinucleotide-repeat expansion in a novel gene. Much has been learned about the molecular genetics of Huntington's disease and the possible effects of the trinucleotide expansion in the development of this disease and other neurological disorders. The Huntington's(More)
Magnetic bead capture utilizes biotin-streptavidin magnetic bead technology to isolate cDNAs rapidly from large genomic intervals, giving several thousand-fold enrichment of the selected cDNAs. The technique can allow parallel analysis of several large genomic segments of varying complexities and can be applied to the isolation of expressed sequences from(More)
Huntington's disease is due to an expansion of CAG repeats in the huntingtin gene. Huntingtin interacts with several proteins including glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We performed immunohistochemical analysis of GAPDH expression in the brains of transgenic mice carrying the huntingtin gene with 89 CAG repeats. In all wild-type animals(More)
We report the identification of a full-length novel beta-spectrin II gene (betaSpIIsigma2) in human brain. The betaSpIIsigma2 gene has 32 exons encoding an actin-binding domain, followed by 17-spectrin repeats, and a short COOH-terminal regulatory region that lacks the Pleckstrin homology (PH) domain. Pair-wise sequence analysis showed an additional 36 and(More)
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