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Mol. Cells 2010; 30(1): 1-12

Published online July 14, 2010

https://doi.org/10.1007/s10059-010-0105-0

© The Korean Society for Molecular and Cellular Biology

Reactive Oxygen Species in TNFalpha-Induced Signaling and Cell Death

Michael J. Morgan, and Zheng-gang Liu*

Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA

Correspondence to : *Correspondence: zgliu@helix.nih.gov

Received: June 14, 2010; Accepted: June 17, 2010

Abstract

TNFα is a pleotropic cytokine that initiates many down-stream signaling pathways, including NF-κB activation, MAP kinase activation and the induction of both apop-tosis and necrosis. TNFα has shown to lead to reactive oxygen species generation through activation of NADPH oxidase, through mitochondrial pathways, or other en-zymes. As discussed, ROS play a role in potentiation or inhibition of many of these signaling pathways. We par-ticularly discuss the role of sustained JNK activation potentiated by ROS, which generally is supportive of apoptosis and "necrotic cell death" through various mechanisms, while ROS could have inhibitory or stimulatory roles in NF-κB signaling.

Keywords JNK, necrotic cell death, NF-κB, ROS, TNFα

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Mol. Cells 2010; 30(1): 1-12

Published online July 31, 2010 https://doi.org/10.1007/s10059-010-0105-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Reactive Oxygen Species in TNFalpha-Induced Signaling and Cell Death

Michael J. Morgan, and Zheng-gang Liu*

Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA

Correspondence to:*Correspondence: zgliu@helix.nih.gov

Received: June 14, 2010; Accepted: June 17, 2010

Abstract

TNFα is a pleotropic cytokine that initiates many down-stream signaling pathways, including NF-κB activation, MAP kinase activation and the induction of both apop-tosis and necrosis. TNFα has shown to lead to reactive oxygen species generation through activation of NADPH oxidase, through mitochondrial pathways, or other en-zymes. As discussed, ROS play a role in potentiation or inhibition of many of these signaling pathways. We par-ticularly discuss the role of sustained JNK activation potentiated by ROS, which generally is supportive of apoptosis and "necrotic cell death" through various mechanisms, while ROS could have inhibitory or stimulatory roles in NF-κB signaling.

Keywords: JNK, necrotic cell death, NF-κB, ROS, TNFα

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
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Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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