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CELL GROWTH AND DEVELOPMENT

Essential Roles of Receptor-Interacting Protein and TRAF2 in Oxidative Stress-Induced Cell Death

Han-Ming Shen, Yong Lin, Swati Choksi, Jamie Tran, Tian Jin, Lufen Chang, Michael Karin, Jianke Zhang, Zheng-gang Liu
Han-Ming Shen
1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute
2Department of Community, Occupational and Family Medicine, Faculty of Medicine, National University of Singapore, Singapore 117597, Republic of Singapore
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Yong Lin
1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute
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Swati Choksi
1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute
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Jamie Tran
1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute
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Tian Jin
3Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland
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Lufen Chang
4Department of Pharmacology, University of California, San Diego, San Diego, California
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Michael Karin
4Department of Pharmacology, University of California, San Diego, San Diego, California
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Jianke Zhang
5Department of Microbiology & Immunology, Thomas Jefferson University Medical College, Philadelphia, Pennsylvania
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Zheng-gang Liu
1Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute
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  • For correspondence: zgliu@helix.nih.gov
DOI: 10.1128/MCB.24.13.5914-5922.2004
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ABSTRACT

Oxidative stress and reactive oxygen species (ROS) can elicit and modulate various physiological and pathological processes, including cell death. However, the mechanisms controlling ROS-induced cell death are largely unknown. Data from this study suggest that receptor-interacting protein (RIP) and tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2), two key effector molecules of TNF signaling, are essential for ROS-induced cell death. We found that RIP−/− or TRAF2−/− mouse embryonic fibroblasts (MEF) are resistant to ROS-induced cell death when compared to wild-type cells, and reconstitution of RIP and TRAF2 gene expression in their respective deficient MEF cells restored their sensitivity to H2O2-induced cell death. We also found that RIP and TRAF2 form a complex upon H2O2 exposure, but without the participation of TNFR1. The colocalization of RIP with a membrane lipid raft marker revealed a possible role of lipid rafts in the transduction of cell death signal initiated by H2O2. Finally, our results demonstrate that activation of c-Jun NH2-terminal kinase 1 is a critical event downstream of RIP and TRAF2 in mediating ROS-induced cell death. Therefore, our study uncovers a novel signaling pathway regulating oxidative stress-induced cell death.

  • Copyright © 2004 American Society for Microbiology
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Essential Roles of Receptor-Interacting Protein and TRAF2 in Oxidative Stress-Induced Cell Death
Han-Ming Shen, Yong Lin, Swati Choksi, Jamie Tran, Tian Jin, Lufen Chang, Michael Karin, Jianke Zhang, Zheng-gang Liu
Molecular and Cellular Biology Jun 2004, 24 (13) 5914-5922; DOI: 10.1128/MCB.24.13.5914-5922.2004

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Essential Roles of Receptor-Interacting Protein and TRAF2 in Oxidative Stress-Induced Cell Death
Han-Ming Shen, Yong Lin, Swati Choksi, Jamie Tran, Tian Jin, Lufen Chang, Michael Karin, Jianke Zhang, Zheng-gang Liu
Molecular and Cellular Biology Jun 2004, 24 (13) 5914-5922; DOI: 10.1128/MCB.24.13.5914-5922.2004
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KEYWORDS

oxidative stress
Proteins

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