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Reactive oxygen species and the neuronal fate

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Abstract

Aberrant or elevated levels of reactive oxygen species (ROS) can mediate deleterious cellular effects, including neuronal toxicity and degeneration observed in the etiology of a number of pathological conditions, including Alzheimer’s and Parkinson’s diseases. Nevertheless, ROS can be generated in a controlled manner and can regulate redox sensitive transcription factors such as NFκB, AP-1 and NFAT. Moreover, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional networks and signaling cascades important for neurogenesis. A large body of literature links the controlled generation of ROS at low-to-moderate levels with the stimulation of differentiation in certain developmental programs such as neurogenesis. In this regard, ROS are involved in governing the acquisition of the neural fate—from neural induction to the elaboration of axons. Here, we summarize and discuss the growing body of literature that describe a role for ROS signaling in neuronal development.

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Acknowledgements

Work from the authors’ laboratory was supported by grants (to S.S.C.L.) from the Canadian Institute of Health Research and the Canadian Cancer Society. S.C.C.L. holds a Canada Research Chair in Functional Genomics and Cellular Proteomics.

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Correspondence to Shawn S.-C. Li.

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K.A.M. Kennedy and S.D.E. Sandiford contributed equally to this work.

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Kennedy, K.A.M., Sandiford, S.D.E., Skerjanc, I.S. et al. Reactive oxygen species and the neuronal fate. Cell. Mol. Life Sci. 69, 215–221 (2012). https://doi.org/10.1007/s00018-011-0807-2

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