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Abstract

Reactive oxygen species (ROS) have been implicated in the pathogenesis of several human diseases, including adult respiratory distress syndrome, myocardial infarction, and Parkinson’s disease.1,2 ROS produce a variety of effects on tissues, including both stimulation and inhibition of cell growth, cell death (both necrotic and apoptotic), and the expression of novel genes involved in cellular repair and antioxidant defenses.3,4 The signal transduction pathways that mediate these responses are now beginning to be elucidated. Work in both prokaryotes and eukaryotes has led to the concept that oxidative stress is itself a second messenger pathway utilized by cells in their vital signaling processes.5-7 Oxidative stress is thought to alter gene expression in part by activating latent transcription factors and several immediate early genes, such as c-myc and c-fos. 8,9 As noted in prior chapters, NF-κB and AP-1 are examples of transcription factors involved in immediate early gene expression that are also activated by ROS.5,10 Recent work in our laboratory indicates that the STAT family of transcription factors (signal transducers and activators of transcription) are activated by ROS.11,12 This chapter provides background on the STAT signal transduction pathway and discusses some newly emerging data about the role of the STAT signal transduction pathway in mediating the cell’s transcriptional response to oxidative stress.

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Simon, A.R., Fanburg, B.L., Cochran, B.H. (1997). STAT Activation by Oxidative Stress. In: Forman, H.J., Cadenas, E. (eds) Oxidative Stress and Signal Transduction. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5981-8_11

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  • DOI: https://doi.org/10.1007/978-1-4615-5981-8_11

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