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• W2011035933 startingPage "182" @default.
• W2011035933 abstract "Huntington's disease is characterized by a loss of brain striatal neurons that occurs as a consequence of an expansion of a CAG repeat in the huntingtin protein. The resulting extended polyglutamine stretch confers a deleterious gain-of-function to the protein. Analysis of the mutant protein has attracted most of the research activity in the field, however re-examination of earlier data and new results on the beneficial functions of normal huntingtin indicate that loss of the normal protein function might actually equally contribute to the pathology. Thus, complete elucidation of the physiological role(s) of huntingtin and its mode of action are essential and could lead to new therapeutic approaches." @default.
• W2011035933 created "2016-06-24" @default.
• W2011035933 creator A5013512498 @default.
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• W2011035933 creator A5070728855 @default.
• W2011035933 creator A5086814591 @default.
• W2011035933 date "2001-03-01" @default.
• W2011035933 modified "2023-10-11" @default.
• W2011035933 title "Loss of normal huntingtin function: new developments in Huntington's disease research" @default.
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• W2011035933 doi "https://doi.org/10.1016/s0166-2236(00)01721-5" @default.
• W2011035933 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11182459" @default.
• W2011035933 hasPublicationYear "2001" @default.

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