title: Reactive oxygen species in TNFalpha-induced signaling and cell death.
abstract: TNFalpha is a pleotropic cytokine that initiates many downstream signaling pathways, including NF-kappaB activation, MAP kinase activation and the induction of both apoptosis and necrosis. TNFalpha has shown to lead to reactive oxygen species generation through activation of NADPH oxidase, through mitochondrial pathways, or other enzymes. As discussed, ROS play a role in potentiation or inhibition of many of these signaling pathways. We particularly 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-kappaB signaling.
authors.affiliation: Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Morgan
authors.forename: Zheng-Gang
authors.initials: ZG
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D016923:Cell Death / Q000502:physiology*; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism* / Q000494:pharmacology
chemical_list: D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha