ROS (reactive oxygen species) have long been regarded as a series of destructive molecules that have a detrimental effect on cell homoeostasis. In support of this are the myriad antioxidant defence systems nearly all eukaryotic cells have that are designed to keep the levels of ROS in check. However, research data emerging over the last decade have demonstrated that ROS can influence a range of cellular events in a manner similar to that seen for traditional second messenger molecules such as cAMP. Hydrogen peroxide (H2O2) appears to be the main ROS with such signalling properties, and this molecule has been shown to affect a wide range of cellular functions. Its localized synthesis by the Nox (NADPH oxidase) family of enzymes and how these enzymes are regulated is of particular interest to those who work in the field of tumour biology.
- hydrogen peroxide (H2O2)
- NADPH oxidase (Nox)
- reactive oxygen species (ROS)
Redox Regulation in Health and Disease: a Celebration of 50 Years of the Keilin Memorial Lecture: A Biochemical Society Focused Meeting held at The Royal Society, Edinburgh, U.K., 19–21 March 2014. Organized and Edited by Colin Campbell (University of Edinburgh, U.K.), Ian Megson (University of the Highlands and Islands, U.K.) and Mark Miller (University of Edinburgh, U.K.).
Abbreviations: BCR, breakpoint cluster region; Duox, dual oxidase; ERK, extracellular-signal-regulated kinase; FLT3-ITD, Fms-like tyrosine kinase internal tandem duplication; JAK, Janus kinase; MEK, mitogen-activated protein kinase/ERK kinase; Nox, NADPH oxidase; PI3K, phosphoinositide 3-kinase; PP, protein phosphatase; Prx, peroxiredoxin; PTEN, phosphatase and tensin homologue deleted on chromosome 10; PTP, protein tyrosine phosphatase; ROS, reactive oxygen species; SHP, Src homology region 2 domain-containing phosphatase; SOD, superoxide dismutase; STAT, signal transducer and activator of transcription
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