Redox Regulation of Cell Survival
By D. Trachootham, Weiqin Lu, Marcia A. Ogasawara, Nilsa Rivera-Del Valle, Peng Huang. Antioxidants and Redox Signaling, 2008
1,755 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0dd47b6e13264d51cd6baf40a025e3b3b3115b89
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In Molecular Biology
- D. Trachootham
- Peng Huang
- K. Davies
- H. Forman
- Erin R Green
- G. T. Nguyen
- Johannes A. Schmid
- J. Alexandre
Citations in the corpus
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling (2018, neutral): “Acting in concert with receptor tyrosine kinases, PTPs play a regulatory role in many cellular functions such as responses to growth factor signaling (Trachootham et al., 2008).”
- How Do Nutritional Antioxidants Really Work: Nucleophilic Tone and Para-Hormesis Versus Free Radical Scavenging in vivo (2013, positive): “In this respect, the shared crucial common motif in cell signaling, is the formation of redox signaling molecules (H2O2, lipid hydroperoxides, α,β-unsaturated carbonyls, and possibly other electrophiles) that activate a series of redox switches through oxidation of specific cysteine residues [121, 1”
- Reactive oxygen species (ROS) and wound healing: the functional role of ROS and emerging ROS‐modulating technologies for augmentation of the healing process (2017, background): “are cytostatic), ii basal ROS levels maintain normal cell functioning and homeostasis, iii increased amounts induce a number of transcription factors to drive a cell-mediated defence response and iv excessive ROS induction activates pro-apoptotic proteins for subsequent induction of cell death, and ”
- The complexity of NF-κB signaling in inflammation and cancer (2013, background): “These compounds react quickly with many other substances leading to their oxidation and they can even react with nitrogen dissolved in the aqueous environment generating so called reactive nitrogen species (RNS), which themselves lead to nitrosylations [141].”
- Oxidative Stress, Prooxidants, and Antioxidants: The Interplay (2014, background): “Any alteration in homeostasis leads to an increased production of these free radicals, much above the detoxifying capability of the local tissues [23].”
- Regulation of µ-Opioid Receptors: Desensitization, Phosphorylation, Internalization, and Tolerance (2013, background): “The role of ROS and redox homeostasis in regulation of cell growth and survival has been intensively investigated in numerous studies (reviewed by Trachootham et al., 2008).”
- Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance (2017, background): “Extensive damage can contribute to tissue injury, neurodegeneration, carcinogenesis, and aging (Trachootham et al., 2008; O’Neill et al., 2015).”
- Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review (2014, background): “While MDA can react with DNA bases, resulting in gene mutations, HNE reacts mostly with proteins, leading to functional alterations [83].”
- Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? (2009, background): “ROS can modulate the activities and expression of many transcription factors and signalling proteins that are involved in the stress response and cell survival through multiple mechanism”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Oxidative stress occurs when there is a disturbance in this pro-oxidant:antioxidant balance and it has been implicated in several biological and pathological processes [186].”
- Anoikis molecular pathways and its role in cancer progression. (2013, background): “Several stimuli can induce the phosphorylation and dissociation of IκB from NF-κB, which migrates into the nucleus and induces expression of anti-apoptotic proteins, such as Bcl-xL and XIAP [226].”
- The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “However, this increases the oxidative state in the cell, and resulting in a homeostatic disruption of the redox balance, cell damage, and apoptosis [117, 118].”