Experimental therapeutics in transgenic mouse models of Huntington's disease
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Neuroscience
Link
http://www.nature.com/articles/nrn1386.pdf
Reference142 articles.
1. Huntington, G. On chorea. Med. Surg. Rep. 26, 317–321 (1872).
2. The Huntington's Disease Collaborative Research Group. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. Cell 72, 971–983 (1993).
3. Gunawardena, S. et al. Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ in Drosophila. Neuron 40, 25–40 (2003). A well-done study showing that overexpression of pathologic polyQ in D. melanogaster disrupts fast axonal transport and that this precedes transcriptional dysfunction.
4. Szebenyi, G. et al. Neuropathogenic forms of huntingtin and androgen receptor inhibit fast axonal transport. Neuron 40, 41–52 (2003). Evidence that mutant polyglutamine-containing proteins directly inhibit fast axonal transport in isolated axoplasm from squid giant axons.
5. Trushina, E. et al. Microtubule destabilization and nuclear entry are sequential steps leading to toxicity in Huntington's disease. Proc. Natl Acad. Sci. USA 21, 12171–12176 (2003).
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