Cytosolic caspases mediate mislocalised SOD2 depletion in an in vitro model of chronic prion infection

SUMMARY 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 pr...

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Bibliographic Details
Main Authors: Layla Sinclair, Victoria Lewis, Steven J. Collins, Cathryn L. Haigh
Format: Article
Language:English
Published: The Company of Biologists 2013-07-01
Series:Disease Models & Mechanisms
Online Access:http://dmm.biologists.org/content/6/4/952