| Progressive depletion of complexin II in a transgenic mouse model of Huntington's disease. | |
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MedLine Citation:
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PMID: 11145989 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor, emotional and cognitive dysfunction. There is no treatment or cure for this disease, and after the onset of symptoms, usually in the fourth decade of life, there is an inexorable decline to death. In many patients there is a complex deterioration of function before the onset of neuronal loss and, at least in mouse models, abnormalities in neurotransmission represent early events in the development of the disease. Here we describe the specific and progressive loss of complexin II from the brains of mice carrying the HD mutation (R6/2 line), and the later appearance of this protein in a subpopulation of neuronal intranuclear inclusions. Although the precise role of complexin II is still unclear, it is known to bind to the SNARE complex, and is therefore likely to be involved in the control of exocytosis. Our results suggest that changes in neurotransmitter release might contribute to the neuronal dysfunction seen in these mice. |
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Authors:
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A J Morton; J M Edwardson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neurochemistry Volume: 76 ISSN: 0022-3042 ISO Abbreviation: J. Neurochem. Publication Date: 2001 Jan |
Date Detail:
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Created Date: 2001-01-23 Completed Date: 2001-02-08 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 166-72 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, University of Cambridge, Cambridge, UK. ajm41@cam.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Vesicular Transport Aging / metabolism Animals Brain / metabolism, pathology Carrier Proteins / metabolism Cell Nucleus / metabolism, ultrastructure Disease Models, Animal Disease Progression Huntington Disease / metabolism*, pathology Inclusion Bodies / metabolism Membrane Proteins / metabolism Mice Mice, Transgenic Nerve Tissue Proteins / deficiency*, metabolism* Organ Specificity SNARE Proteins Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins Synaptic Transmission Synaptic Vesicles / metabolism Vesicular Transport Proteins* |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Vesicular Transport; 0/Carrier Proteins; 0/Membrane Proteins; 0/Nerve Tissue Proteins; 0/SNARE Proteins; 0/Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins; 0/Vesicular Transport Proteins; 0/complexin II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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