Oxidant Sensing by Reversible Disulfide Bond Formation

Cremers, Claudia M.; Jakob, Ursula

doi:10.1074/jbc.r113.462929

Cited by 362 publications

(284 citation statements)

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“…inactivated phosphatases were hypothesized to shift the equilibrium of inactive to active kinases resulting in enhanced kinase activity (18,25,26). By now, a large number of redox modifications in phosphatases, kinases, adapters, receptors, and transcription factors have been proposed to modulate signaling, among them multiple components of the BCR signaling pathway such as tyrosine-protein kinase Lyn, tyrosine-protein kinase SYK (Syk), tyrosine-protein phosphatase nonreceptor types 6 and 11 (SHP1/PTPN6; SHP2/PTPN11), phosphatase and tensin homolog, and a mitogen activated protein (MAP) kinase serine/threonine phosphatase (27)(28)(29)(30)(31)(32)(33)(34)(35)(36). However, it has been challenging to prove or disprove the physiological relevance of such a mechanism, and results have been difficult to reconcile as a whole (3,26,35).…”

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confidence: 99%

A respiratory chain controlled signal transduction cascade in the mitochondrial intermembrane space mediates hydrogen peroxide signaling

Patterson

Gerbeth

Thiru

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) govern cellular homeostasis by inducing signaling. H2O2 modulates the activity of phosphatases and many other signaling molecules through oxidation of critical cysteine residues, which led to the notion that initiation of ROS signaling is broad and nonspecific, and thus fundamentally distinct from other signaling pathways. Here, we report that H2O2 signaling bears hallmarks of a regular signal transduction cascade. It is controlled by hierarchical signaling events resulting in a focused response as the results place the mitochondrial respiratory chain upstream of tyrosine-protein kinase Lyn, Lyn upstream of tyrosine-protein kinase SYK (Syk), and Syk upstream of numerous targets involved in signaling, transcription, translation, metabolism, and cell cycle regulation. The active mediators of H2O2 signaling colocalize as H2O2 induces mitochondria-associated Lyn and Syk phosphorylation, and a pool of Lyn and Syk reside in the mitochondrial intermembrane space. Finally, the same intermediaries control the signaling response in tissues and species responsive to H2O2 as the respiratory chain, Lyn, and Syk were similarly required for H2O2 signaling in mouse B cells, fibroblasts, and chicken DT40 B cells. Consistent with a broad role, the Syk pathway is coexpressed across tissues, is of early metazoan origin, and displays evidence of evolutionary constraint in the human. These results suggest that H2O2 signaling is under control of a signal transduction pathway that links the respiratory chain to the mitochondrial intermembrane space-localized, ubiquitous, and ancient Syk pathway in hematopoietic and nonhematopoietic cells.

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confidence: 99%

A respiratory chain controlled signal transduction cascade in the mitochondrial intermembrane space mediates hydrogen peroxide signaling

Patterson

Gerbeth

Thiru

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…ROS transiently modulate protein activity by protein modification, most commonly via the formation of disulfide bonds. [10][11][12] Recent studies suggest that thiol exchange pathways involving protein disulfide isomerase (PDI) regulate TF activation via reversible disulfide bond formation. [13][14][15][16] Wang et al 17 showed that thioredoxin (Trx) knockdown caused a significant increase in cell surface TF procoagulant activity in MDA-MB-231 cells, indicating that the thioredoxin reductase (TrxR)/Trx system negatively regulates TF coagulant activity.…”

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confidence: 99%

The lipid peroxidation product 4-hydroxy-2-nonenal induces tissue factor decryption via ROS generation and the thioredoxin system

2017

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“…The redox state inside the ER lumen is highly oxidant and the changes caused by the presence of ROS afect the correct protein folding. It contributes to the breaking of the disulphide bonds by the binding of reactive species to thiol groups [51]. Misfolded proteins that are formed in the ER cause Ca 2+ release in the cytoplasmic space.…”

Section: Alterations In Endoplasmic Reticulum Function and Signalmentioning

confidence: 99%

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

Rivas‐Arancibia¹,

Rodrı́guez-Martı́nez²,

Méndez‐García³

et al. 2016

Free Radicals and Diseases

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Alzheimer's disease is characterized by the pathognomonic presence of intracellular neuroibrillary tangles containing hyperphosphorylated tau protein and extracellular senile plaques primarily formed by -amyloid. Both the neuroibrillary tangles and the plaques formed by -amyloid 1-42 are the inal result of a chain of events that progressed along with the disease for a long time. Oxidative stress plays a fundamental role among those events as proven by the experiments carried out using animal models. This can be demonstrated since there are studies indicating that, although the formation ofamyloid is inhibited through diferent mechanisms using drugs or speciic antibodies), cognitive deicit is not prevented. In this chapter, we will focus on reviewing the role the chronic state of oxidative stress plays in the development of Alzheimer's disease and how the loss of redox balance induces a vicious cycle that may change normal signaling. As a consequence, there are alterations in multiple metabolic pathways that end up in the formation of hyperphosphorylated tau and insoluble -amyloid, leading to the advance of a progressive neurodegeneration process. This is characterized by neuronal dead, astrocytic changes, microglia activation, and the loss of brain repair.Keywords: oxidative stress, Alzheimer's disease, -amyloid 1-42, ozone, neurodegeneration © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. . IntroductionDespite a great deal of studies and the eforts of researchers in the ield, the physiopathology of Alzheimer's disease AD) is not yet clear. There is neither an accurate early diagnosis nor an efective treatment that allows the patients to have beter life expectancies [1]. Perhaps one of the most important problems to solve is understand that when the diagnosis is made, the symptoms and the signs of Alzheimer's disease are the result of a long chain of events that took place during an extended period of time and that such symptoms and signs change with time [2].One can assume that intracellular signaling and metabolic changes found during the early stages of the disease are not the same as the ones found at more advanced stages. For this reason, recent postmortem studies fail to completely clarify the physiopathology of this disease. . Changes at cellular level caused by chronic oxidative stressAcute oxidative stress is reversible and it is present in a number of physiological and pathological mechanisms that are reversible as well. These mechanisms play a defensive role ...

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Oxidant Sensing by Reversible Disulfide Bond Formation

Cited by 362 publications

References 100 publications

A respiratory chain controlled signal transduction cascade in the mitochondrial intermembrane space mediates hydrogen peroxide signaling

A respiratory chain controlled signal transduction cascade in the mitochondrial intermembrane space mediates hydrogen peroxide signaling

The lipid peroxidation product 4-hydroxy-2-nonenal induces tissue factor decryption via ROS generation and the thioredoxin system

Oxidative Stress, Inflammation, and Formation of Beta‐ Amyloid 1‐42 in Brain

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