title: Reactive oxygen species and the neuronal fate.
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.
authors.affiliation: Department of Biochemistry, Medical Sciences Building, The University of Western Ontario, London, ON, Canada.
authors.forename: Karen A M
authors.initials: KA
authors.lastname: Kennedy
authors.forename: Shelley D E
authors.initials: SD
authors.lastname: Sandiford
authors.forename: Ilona S
authors.initials: IS
authors.lastname: Skerjanc
authors.forename: Shawn S-C
authors.initials: SS
authors.lastname: Li
mesh_terms: D000818:Animals; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D019255:NADPH Oxidases / Q000378:metabolism; D009420:Nervous System / Q000254:growth & development / Q000378:metabolism*; D055495:Neurogenesis; D009474:Neurons / Q000201:enzymology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases