Journal
TRENDS IN GENETICS
Volume 20, Issue 3, Pages 146-154Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tig.2004.01.008
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Funding
- NIA NIH HHS [AG19206] Funding Source: Medline
- NINDS NIH HHS [NS41669, NS36232] Funding Source: Medline
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At least nine inherited neurodegenerative diseases share a polyglutamine expansion in their respective disease proteins. These diseases show distinct neuropathological changes, suggesting that protein environment and protein-protein interactions play an important role in the specific neuropathology. A gain of toxic function as a result of an expanded polyglutamine tract can cause the protein huntingtin to interact abnormally with a variety of proteins, resulting in the complex of neuropathological changes seen in Huntington's disease. Recent studies have identified several huntingtin-interacting proteins that might be associated with the normal function of huntingtin and/or involved in the pathology of Huntington's disease. In this article, we focus on the potential roles of huntingtin-protein interactions in the pathogenesis of Huntington's disease.
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