Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease-Reference-Cited by-同舟云学术

Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease

Published:2002-10-07 Issue:3 Volume:32 Page:420-425
ISSN:1061-4036
Container-title:Nature Genetics
language:en
Short-container-title:Nat Genet

Author:

Wilson Scott M.,Bhattacharyya Bula,Rachel Rivka A.,Coppola Vincenzo,Tessarollo Lino,Householder Deborah B.,Fletcher Colin F.,Miller Richard J.,Copeland Neal G.,Jenkins Nancy A.

Publisher

Springer Science and Business Media LLC

Subject

Genetics

Link

http://www.nature.com/articles/ng1006z.pdf

Reference30 articles.

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2. Yin, L., Krantz, B., Russell, N.S., Deshpande, S. & Wilkinson, K.D. Nonhydrolyzable diubiquitin analogues are inhibitors of ubiquitin conjugation and deconjugation. Biochemistry 39, 10001–10010 (2000).

3. McNaught, K.S., Olanow, C.W., Halliwell, B., Isacson, O. & Jenner, P. Failure of the ubiquitin–proteasome system in Parkinson's disease. Nat. Rev. Neurosci. 2, 589–594 (2001).

4. Skinner, P.J. et al. Ataxin-1 with an expanded glutamine tract alters nuclear matrix-associated structures. Nature 389, 971–974 (1997).

5. Saigoh, K. et al. Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice. Nat. Genet. 23, 47–51 (1999).

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