2021
DOI: 10.1016/j.jbc.2021.100388
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Regulation of ATR-dependent DNA damage response by nitric oxide

Abstract: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, a… Show more

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Cited by 6 publications
(3 citation statements)
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References 83 publications
(127 reference statements)
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“…In case of higher energy demand and increased neuronal activity such as in stress, hypoxia, inflammation/injury, and NMDA stimulation, Ca transients together with the 5' AMP-activated protein kinase (AMPK) cascade lead to increased glycolysis and catabolic processes (e.g., fatty acid oxidation) and induction of the inducible isoform of nitric oxide synthase (iNOS) in order to sustain neuronal activity [55]. iNOS induction leads to dysregulation of the NO equilibrium, ONOO − formation, and GSH trafficking decline, collectively causing mitochondrial damage via ROS/RNS generation [56]. Apart from NO, other components of the oxidative phosphorylation cascade such as the HO-1 and GSH pathways and lipid oxidation products (e.g., 4-hydroxynonenal, 4-HNE) are also involved in the generation of ROS (i.e., through pro-oxidant Fe generation) and the promotion of autophagy, senescence, cell cycle arrest, apoptosis, and cell death [57][58][59][60].…”
Section: Redox System Components 241 Nitric Oxide (No) and The Oxidative Phosphorylation Cascadementioning
confidence: 99%
“…In case of higher energy demand and increased neuronal activity such as in stress, hypoxia, inflammation/injury, and NMDA stimulation, Ca transients together with the 5' AMP-activated protein kinase (AMPK) cascade lead to increased glycolysis and catabolic processes (e.g., fatty acid oxidation) and induction of the inducible isoform of nitric oxide synthase (iNOS) in order to sustain neuronal activity [55]. iNOS induction leads to dysregulation of the NO equilibrium, ONOO − formation, and GSH trafficking decline, collectively causing mitochondrial damage via ROS/RNS generation [56]. Apart from NO, other components of the oxidative phosphorylation cascade such as the HO-1 and GSH pathways and lipid oxidation products (e.g., 4-hydroxynonenal, 4-HNE) are also involved in the generation of ROS (i.e., through pro-oxidant Fe generation) and the promotion of autophagy, senescence, cell cycle arrest, apoptosis, and cell death [57][58][59][60].…”
Section: Redox System Components 241 Nitric Oxide (No) and The Oxidative Phosphorylation Cascadementioning
confidence: 99%
“…The characteristic of NO with radical electrons (lone pair electrons) endows it with reactivity to inorganic molecules (oxygen, superoxide or transition metal), prosthetic groups and DNA structure, thus depicting its wide range of biological activities 19 . The effect of NO is mainly mediated through two methods: cyclic guanosine phosphate (cGMP)-dependent and cGMP-independent.…”
Section: Introductionmentioning
confidence: 99%
“…Such reactivity could be ascribed to either cGMP-dependent or cGMP-independent physiological pathways. 29 Several studies report different mechanisms like inhibition of HIF 1α, 30 mitochondrial respiration, 31 and or DNA synthesis for anticancer effects, and we will surely aim at exploring the mechanism of our results in future studies. We would also like to design combinatorial therapy with nonconventional systems 25 like immunotherapy, PDT (photodynamic therapy), or PTT (photothermal therapy) and work towards overcoming multidrug resistance with NO donor derivatives in the future.…”
mentioning
confidence: 96%