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• W2128517811 endingPage "492" @default.
• W2128517811 startingPage "475" @default.
• W2128517811 abstract "Huntington disease (HD) is a neurodegenerative disorder caused by an elongated polyglutamine tract in huntingtin (htt). htt normally undergoes different posttranslational modifications (PTMs), including phosphorylation, SUMOylation, ubiquitination, acetylation, proteolytic cleavage, and palmitoylation. In the presence of the HD mutation, some PTMs are significantly altered and can result in changes in the clinical phenotype. A rate-limiting PTM is defined as one that can result in significant effects on the phenotype in animal models. For example, the prevention of proteolysis at D586 as well as constitutive phosphorylation at S13 and S16 can obviate the expression of phenotypic features of HD. The enzymes involved in these modifications such as caspase-6, the IκB kinase (IKK) complex, and still to be characterized phosphatases therefore represent promising therapeutic targets for HD. Identifying and testing specific modulators of PTMs now constitute the next big challenges in order to further validate these targets and proceed towards the goal of a mechanism-based treatment for HD." @default.
• W2128517811 created "2016-06-24" @default.
• W2128517811 creator A5006854193 @default.
• W2128517811 creator A5047722409 @default.
• W2128517811 creator A5064706026 @default.
• W2128517811 date "2011-02-10" @default.
• W2128517811 modified "2023-10-01" @default.
• W2128517811 title "Small Changes, Big Impact" @default.
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