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• W2019581652 abstract "CAG/polyglutamine expansion is the mutational mechanism that causes a number of late-onset neurodegenerative diseases. Expanded CAG repeats are unstable: they vary in size between tissues and change in size upon transmission from parent to offspring. These mutations are thought to impact a dominant gain of function to the proteins in which they are located. Recent reports describing the first mouse models of these diseases promise to shed light on the molecular mechanisms underlying CAG-repeat instability, the pathways by which polyglutamine expansion causes cell death and the factors that determine the specificity of the neurodegeneration. CAG/polyglutamine expansion is the mutational mechanism that causes a number of late-onset neurodegenerative diseases. Expanded CAG repeats are unstable: they vary in size between tissues and change in size upon transmission from parent to offspring. These mutations are thought to impact a dominant gain of function to the proteins in which they are located. Recent reports describing the first mouse models of these diseases promise to shed light on the molecular mechanisms underlying CAG-repeat instability, the pathways by which polyglutamine expansion causes cell death and the factors that determine the specificity of the neurodegeneration." @default.
• W2019581652 created "2016-06-24" @default.
• W2019581652 creator A5020296130 @default.
• W2019581652 creator A5060895838 @default.
• W2019581652 date "1997-11-01" @default.
• W2019581652 modified "2023-10-11" @default.
• W2019581652 title "Transgenic mouse models of neurodegenerative disease caused by CAG/polyglutamine expansions" @default.
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• W2019581652 doi "https://doi.org/10.1016/s1357-4310(97)01142-8" @default.
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