Allele-specific RNAi selectively silences mutant SOD1 and achieves significant therapeutic benefit in vivo
- 30 September 2006
- journal article
- Published by Elsevier BV in Neurobiology of Disease
- Vol. 23 (3), 578-586
- https://doi.org/10.1016/j.nbd.2006.04.019
Abstract
No abstract availableKeywords
This publication has 43 references indexed in Scilit:
- Silencing Primary Dystonia: Lentiviral-Mediated RNA Interference Therapy for DYT1 DystoniaJournal of Neuroscience, 2005
- RNA interference improves motor and neuropathological abnormalities in a Huntington's disease mouse modelProceedings of the National Academy of Sciences of the United States of America, 2005
- CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in lifeOncogene, 2004
- siRNA relieves chronic neuropathic painNucleic Acids Research, 2004
- Selective silencing by RNAi of a dominant allele that causes amyotrophic lateral sclerosisAging Cell, 2003
- Induction of an interferon response by RNAi vectors in mammalian cellsNature Genetics, 2003
- ALS-associated mutant SOD1G93A causes mitochondrial vacuolation by expansion of the intermembrane space and by involvement of SOD1 aggregation and peroxisomesBMC Neuroscience, 2003
- In vitro photochemical cataract in mice lacking copper-zinc superoxide dismutaseFree Radical Biology & Medicine, 2001
- Hindlimb Motor Neurons Require Cu/Zn Superoxide Dismutase for Maintenance of Neuromuscular JunctionsThe American Journal of Pathology, 1999
- Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS)Brain Research, 1995