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Cytosolic caspases mediate mislocalised SOD2 depletion in an in vitro model of chronic prion infection
Oxidative stress as a contributor to neuronal death during prion infection is supported by the fact that various oxidative damage markers accumulate in the brain during the course of this disease. The normal cellular substrate of the causative agent, the prion protein, is also linked with protective...
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Main Authors: | , , , |
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格式: | Artigo |
語言: | Inglês |
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The Company of Biologists Limited
2013
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在線閱讀: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3701215/ https://ncbi.nlm.nih.gov/pubmed/23580200 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1242/dmm.010678 |
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