Activation of the Nrf2–ARE pathway in muscle and spinal cord during ALS-like pathology in mice expressing mutant SOD1
- 12 June 2007
- journal article
- Published by Elsevier
- Vol. 207 (1) , 107-117
- https://doi.org/10.1016/j.expneurol.2007.05.026
Abstract
No abstract availableKeywords
This publication has 53 references indexed in Scilit:
- Protein Oxidative Damage in a Transgenic Mouse Model of Familial Amyotrophic Lateral SclerosisJournal of Neurochemistry, 1998
- Aggregation and Motor Neuron Toxicity of an ALS-Linked SOD1 Mutant Independent from Wild-Type SOD1Science, 1998
- Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALSGlia, 1998
- Relationship of oxygen radical-induced lipid peroxidative damage to disease onset and progression in a transgenic model of familial ALSJournal of Neuroscience Research, 1998
- Neuromuscular function impairment is not caused by motor neurone loss in FALS miceNeuroReport, 1996
- Parallel Induction of Heme Oxygenase-1 and Chemoprotective Phase 2 Enzymes by Electrophiles and Antioxidants: Regulation by Upstream Antioxidant-Responsive Elements (ARE)Molecular Medicine, 1995
- Two novel mutations in the gene for copper zinc superoxide dismutase in UK families with amyotrophic lateral sclerosis.1995
- 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
- Familial amyotrophic lateral sclerosis (ALS) in Japan associated with H46R mutation in
Cu Zn Journal of the Neurological Sciences, 1994 - Motor Neuron Degeneration in Mice that Express a Human Cu,Zn Superoxide Dismutase MutationScience, 1994