Radical-free biology of oxidative stress.

By Dean P. Jones. American Journal of Physiology - Cell Physiology, 2008

1,207 citations recorded by the source corpus.

Subfields: Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e74c367f0f4b9fe918460273f7ee2c57c120cdac

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Citations in the corpus

Nox proteins in signal transduction (2009, neutral): “Redox balance—A theory dubbed the “Redox Hypothesis” proposes that redox elements (like redox sensitive cysteine residues) are organized in redox circuits controlled by GSH, thioredoxin and cysteine residues [77].”
Oxidative stress: a concept in redox biology and medicine (2015, methodology): “…citation and similar papers at core.ac.uk provided by Elsevier - Publisher Connector Contents lists available at ScienceDirect Redox Biology http://d 2213-23 E-m journal homepage: www.elsevier.com/locate/redox Mini Review Oxidative stress: a concept in redox biology and medicine Helmut Sies”
Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets (2011, background): “By contrast, it has only recently emerged that excessive ROS production by an overactive NADPH oxidase system, both in phagocytic and non-phagocytic cell types of the artery wall, may set in motion a vicious cycle of radical and non-radical oxidant generation in various cellular compartments, which ”
Redox chemistry of biological thiols (2010, background): “In other words, as a result of marked differences in thiol oxidation and disulfide reduction rates (vis-à-vis catalyzed and noncatalyzed events) the redox status of the cell is controlled kinetically rather than thermodynamically, representing a dynamic nonequilibrium steady-state system [141,142].”
13 reasons why the brain is susceptible to oxidative stress (2018, background): “generate O2 and NO [179,180], so it is unwise to assume NADPH exclusively fuels “antioxidants” [181].”
Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “This is the reason that reactive cysteines are deemed to be the primary molecular switches that are able to transduce a redox signal.(48)”
Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “These data illustrate how the enzymatic action of GPx-1 links it to the intracellular GSH/GSSG redox couple transferring redox stress in the cell to the easily restored GSSG rather than reactive protein thiols (189, 196).”
Mitochondrial Energetics and Therapeutics (2010, positive): “Because TNFα preferentially oxidizes the mitochondrial Trx2(SH)2/(SS), rather than the nucleus-cytosol Trx1(SH)2/(SS) (167), it is possible that ASK1 interacts with both Trx2(SH)2 and Trx1(SH)2 (140, 141).”