SOD-1 inhibits FAS expression in cortex of APP transgenic mice
| Autor: | M. Lepécheur, E. Paly, J. London, J. Zhu, Z. Chen, R.-S. Duan |
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| Rok vydání: | 2005 |
| Předmět: |
Genetically modified mouse
Male Cancer Research Transgene Clinical Biochemistry Pharmaceutical Science Mice Transgenic chemistry.chemical_compound Amyloid beta-Protein Precursor Mice Superoxide Dismutase-1 Alzheimer Disease Glial Fibrillary Acidic Protein Amyloid precursor protein Animals Humans fas Receptor Receptor Gene Pharmacology Cerebral Cortex biology Glial fibrillary acidic protein Chemistry Superoxide Superoxide Dismutase Biochemistry (medical) Cell Biology Molecular biology Apoptosis biology.protein |
| Zdroj: | Apoptosis : an international journal on programmed cell death. 10(3) |
| ISSN: | 1360-8185 |
| Popis: | Peptides derived from proteolytic processing of the amyloid precursor protein (APP) are important for the pathogenesis of Alzheimer's disease (AD). In the present study, we found that transgenic mice overexpressing wild-type human APP gene (hAPP/+) displayed a much higher expression of FAS, one of the death receptor subfamily. This FAS overexpression was significantly reduced in the cortex of mice overexpressing both wild-type hAPP gene and wild-type human superoxide dismutase-1 gene (hSOD-1). Moreover hSOD-1 transgenic expression was associated with an increase of Glial fibrillary acidic protein (GFAP) production. This study indicates that SOD-1 overexpression can inhibit FAS expression, which may be beneficial in AD. |
| Databáze: | OpenAIRE |
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