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Sci. STKE, 21 September 2004
Vol. 2004, Issue 251, p. pe45
[DOI: 10.1126/stke.2512004pe45]

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Emerging Role for ERK as a Key Regulator of Neuronal Apoptosis

Eric C. C. Cheung and Ruth S. Slack*

Ottawa Health Research Institute–Neuroscience Center and Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.

Abstract: Extracellular signal–regulated kinases (ERKs) are traditionally viewed as a survival factor in the mitogen-activated protein kinase (MAPK) family. On the other hand, some recent reports have suggested that ERK can also be responsible for neuronal cell death in various neurodegeneration models. In-depth studies on the action of ERK in apoptosis, however, have not been done. A recent study has revealed that ERK is a key apoptotic factor in potassium deprivation–induced neuronal cell death by showing that ERK inhibitors protect neurons from low potassium conditions, whereas constitutively activated ERK activates cell death. Most important, this study shows how ERK can promote neuronal cell death by causing plasma membrane and DNA damage that is independent of caspase-3 activity. Further studies on the mechanism of ERK in neuronal cell death will shed light on the possibility of using ERK as a therapeutic target in treating neurodegeneration.

*Corresponding author. E-mail: rslack{at}uottawa.ca

Citation: E. C. C. Cheung, R. S. Slack, Emerging Role for ERK as a Key Regulator of Neuronal Apoptosis. Sci. STKE 2004, pe45 (2004).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Mitochondrial dynamics and apoptosis.
D.-F. Suen, K. L. Norris, and R. J. Youle (2008)
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