Journal article

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

Layla Sinclair, Victoria Lewis, Steven J Collins, Cathryn L Haigh

DISEASE MODELS & MECHANISMS | COMPANY OF BIOLOGISTS LTD | Published : 2013

Abstract

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 functions against oxidative stress. Our previous work has found that, in chronic prion infection, an apoptotic subpopulation of cells exhibit oxidative stress and the accumulation of oxidised lipid and protein aggregates with caspase recruitment. Given the likely failure of antioxidant defence mechanisms within apoptotic prion-infected cells, we aimed to investigate the role of the crucial antiox..

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Grants

Awarded by National Health and Medical Research Council (NHMRC)


Funding Acknowledgements

This work was funded by a National Health and Medical Research Council (NH&MRC) program grant (#628946) and a Brain Foundation research grant. S.J.C. is funded by an NH&MRC Practitioner Fellowship (#APP1005816). L.S. is funded in part by a Carol Willesee Foundation Ph.D. scholarship. V.L. is supported by an NH&MRC Training Fellowship (#567123).