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• W1584612115 endingPage "181" @default.
• W1584612115 startingPage "167" @default.
• W1584612115 abstract "The field of redox biology has changed tremendously over the past 20 years. Formerly regarded as bi-products of the aerobic metabolism exclusively involved in tissue damage, reactive oxygen species (ROS) are now recognized as active participants of cell signaling events in health and in disease. In this sense, ROS and the more recently defined reactive nitrogen species (RNS) are, just like hormones and second messengers, acting as fundamental orchestrators of cell signaling pathways. The chemical modification of enzymes by ROS and RNS (that result in functional enzymatic alterations) accounts for a considerable fraction of the transient and persistent perturbations imposed by variations in oxidant levels. Upregulation of ROS and RNS in response to stress is a common cellular response that foments adaptation to a variety of physiologic alterations (hypoxia, hyperoxia, starvation, and cytokine production). Frequently, these are beneficial and increase the organisms' resistance against subsequent acute stress (preconditioning). Differently, the sustained ROS/RNS-dependent rerouting of signaling produces irreversible alterations in cellular functioning, often leading to pathogenic events. Thus, the duration and reversibility of protein oxidations define whether complex organisms remain “electronically” healthy. Among the 20 essential amino acids, four are particularly susceptible to oxidation: cysteine, methionine, tyrosine, and tryptophan. Here, we will critically review the mechanisms, implications, and repair systems involved in the redox modifications of these residues in proteins while analyzing well-characterized prototypic examples. Occasionally, we will discuss potential consequences of amino acid oxidation and speculate on the biologic necessity for such events in the context of adaptative redox signaling. © 2014 IUBMB Life, 66(3):167–181, 2014" @default.
• W1584612115 created "2016-06-24" @default.
• W1584612115 creator A5009563657 @default.
• W1584612115 creator A5013331794 @default.
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• W1584612115 creator A5016460624 @default.
• W1584612115 creator A5045754640 @default.
• W1584612115 creator A5072969548 @default.
• W1584612115 date "2014-03-01" @default.
• W1584612115 modified "2023-10-02" @default.
• W1584612115 title "Redox control of enzymatic functions: The electronics of life's circuitry" @default.
• W1584612115 cites W119600325 @default.
• W1584612115 cites W1233541004 @default.
• W1584612115 cites W1484778273 @default.
• W1584612115 cites W1489145507 @default.
• W1584612115 cites W1523213544 @default.
• W1584612115 cites W1544109218 @default.
• W1584612115 cites W1560777399 @default.
• W1584612115 cites W1713068442 @default.
• W1584612115 cites W1762824323 @default.
• W1584612115 cites W1939083266 @default.
• W1584612115 cites W1965314635 @default.
• W1584612115 cites W1965751588 @default.
• W1584612115 cites W1967236260 @default.
• W1584612115 cites W1969545692 @default.
• W1584612115 cites W1970413507 @default.
• W1584612115 cites W1971202292 @default.
• W1584612115 cites W1972009654 @default.
• W1584612115 cites W1972577475 @default.
• W1584612115 cites W1972989329 @default.
• W1584612115 cites W1973577899 @default.
• W1584612115 cites W1974997758 @default.
• W1584612115 cites W1978296397 @default.
• W1584612115 cites W1979415715 @default.
• W1584612115 cites W1979499161 @default.
• W1584612115 cites W1980385765 @default.
• W1584612115 cites W1981755281 @default.
• W1584612115 cites W1982110121 @default.
• W1584612115 cites W1982287005 @default.
• W1584612115 cites W1982333316 @default.
• W1584612115 cites W1983078193 @default.
• W1584612115 cites W1985745419 @default.
• W1584612115 cites W1986148909 @default.
• W1584612115 cites W1986589519 @default.
• W1584612115 cites W1988998787 @default.
• W1584612115 cites W1993736701 @default.
• W1584612115 cites W1994456301 @default.
• W1584612115 cites W1994769872 @default.
• W1584612115 cites W1995320376 @default.
• W1584612115 cites W1996147899 @default.
• W1584612115 cites W1996235155 @default.
• W1584612115 cites W1996817596 @default.
• W1584612115 cites W1998467336 @default.
• W1584612115 cites W1998572296 @default.
• W1584612115 cites W1999120747 @default.
• W1584612115 cites W1999286346 @default.
• W1584612115 cites W1999365716 @default.
• W1584612115 cites W1999891390 @default.
• W1584612115 cites W1999982239 @default.
• W1584612115 cites W2000155150 @default.
• W1584612115 cites W2004740293 @default.
• W1584612115 cites W2004806037 @default.
• W1584612115 cites W2006026110 @default.
• W1584612115 cites W2007534790 @default.
• W1584612115 cites W2007651247 @default.
• W1584612115 cites W2008613466 @default.
• W1584612115 cites W2012219744 @default.
• W1584612115 cites W2013807298 @default.
• W1584612115 cites W201418494 @default.
• W1584612115 cites W2016693012 @default.
• W1584612115 cites W2016985488 @default.
• W1584612115 cites W2017739035 @default.
• W1584612115 cites W2018895248 @default.
• W1584612115 cites W2019459353 @default.
• W1584612115 cites W2020222238 @default.
• W1584612115 cites W2020536272 @default.
• W1584612115 cites W2021358858 @default.
• W1584612115 cites W2022604438 @default.
• W1584612115 cites W2023017223 @default.
• W1584612115 cites W2023379699 @default.
• W1584612115 cites W2023491051 @default.
• W1584612115 cites W2023632053 @default.
• W1584612115 cites W2023947368 @default.
• W1584612115 cites W2025038110 @default.
• W1584612115 cites W2026254485 @default.
• W1584612115 cites W2026425756 @default.
• W1584612115 cites W2027443731 @default.
• W1584612115 cites W2029808035 @default.
• W1584612115 cites W2029925670 @default.
• W1584612115 cites W2030079903 @default.
• W1584612115 cites W2030647828 @default.
• W1584612115 cites W2030817463 @default.
• W1584612115 cites W2031421173 @default.
• W1584612115 cites W2031699192 @default.
• W1584612115 cites W2032612468 @default.
• W1584612115 cites W2032940945 @default.
• W1584612115 cites W2039241150 @default.
• W1584612115 cites W2039919263 @default.

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