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Cited by 1,792Redox biology and oxidative stressCell death mechanisms and regulationNF-κB Signaling Pathways

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Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase Phosphatases

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Kamata, Hideaki, Honda, Shi-ichi, Maeda, Shin, Chang, Lufen, Hirata, Hajime, Karin, Michael·2005·Cell
DOI 10.1016/j.cell.2004.12.041
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Abstract

TNFalpha is a pleiotropic cytokine that induces either cell proliferation or cell death. Inhibition of NF-kappaB activation increases susceptibility to TNFalpha-induced death, concurrent with sustained JNK activation, an important contributor to the death response. Sustained JNK activation in NF-kappaB-deficient cells was suggested to depend on reactive oxygen species (ROS), but how ROS affect JNK activation was unclear. We now show that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid. This results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage, as well as necrotic cell death. Treatment of cells or experimental animals with an antioxidant prevents H(2)O(2) accumulation, JNK phosphatase oxidation, sustained JNK activity, and both forms of cell death. Antioxidant treatment also prevents TNFalpha-mediated fulminant liver failure without affecting liver regeneration.

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Metadata

Authors
Kamata, H., Honda, S.-I., Maeda, S., Chang, L., Hirata, H., & Karin, M.
Affiliations
  • University of Hyogo (JP)
  • University of California San Diego (US)
Corresponding author
Karin, Michael
ORCID
Venue
Cell
Publisher
Elsevier BV
Published
2005-03
Volume
120
Issue
5
Pages
649-661
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/j.cell.2004.12.041
OpenAlex
W2114111268
Cited by
1,792
References
4
Citations by year
2026: 30 · 2025: 41 · 2024: 49 · 2023: 56 · 2022: 56 · 2021: 82 · 2020: 74 · 2019: 74 · 2018: 65 · 2017: 94 · 2016: 80 · 2015: 88 · 2014: 98 · 2013: 97 · 2012: 94
FWCI
46.93
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5P42 ES10337, AI43477, ES04151, ES06376)
  • Japan Society for the Promotion of Science
  • Ministry of Education, Culture, Sports, Science and Technology (16570121)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
reactive oxygen species, TNF-α, JNK activation, MAP kinase phosphatase, cysteine oxidation, sulfenic acid, mitochondrial superoxide dismutase, NF-κB, cytochrome c release, caspase-3, necrosis, antioxidants, acute liver failure, liver regeneration, oxidative stress
MeSH terms
Animals, Antioxidants, Chlorocebus aethiops, Enzyme Activation, HeLa Cells, Humans, Hydrogen Peroxide, Necrosis, Oxidation-Reduction, Phosphoric Monoester Hydrolases, Sulfenic Acids, Superoxide Dismutase, Tumor Necrosis Factor-alpha, Cell Death, Liver Failure, Acute, Reactive Oxygen Species, Mice, Knockout, Oxidative Stress, COS Cells, Caspases, Cytochromes c, JNK Mitogen-Activated Protein Kinases, Mice, Caspase 3

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