Hsp40 Molecules That Target to the Ubiquitin-proteasome System Decrease Inclusion Formation in Models of Polyglutamine Disease-Reference-Cited by-同舟云学术

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Hsp40 Molecules That Target to the Ubiquitin-proteasome System Decrease Inclusion Formation in Models of Polyglutamine Disease

Published:2007-06 Issue:6 Volume:15 Page:1100-1105
ISSN:1525-0016
Container-title:Molecular Therapy
language:en
Short-container-title:Molecular Therapy

Author:

Howarth JL,Kelly S,Keasey MP,Glover CPJ,Lee Y-B,Mitrophanous K,Chapple JP,Gallo JM,Cheetham ME,Uney JB

Publisher

Elsevier BV

Subject

Drug Discovery,Pharmacology,Genetics,Molecular Biology,Molecular Medicine

Reference43 articles.

1. Variation of the CGG repeat at the fragile X site results in genetic instability: resolution of the Sherman paradox;Fu;Cell,1991

2. Polyglutamines placed into context;La Spada;Neuron,2003

3. Pathogenesis of polyglutamine disorders: aggregation revisited;Michalik;Hum Mol Genet,2003

4. Ectopically expressed CAG repeats cause intranuclear inclusions and a progressive late onset neurological phenotype in the mouse;Ordway;Cell,1997

5. A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration;Hodgson;Neuron,1999

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