Please use this identifier to cite or link to this item: https://doi.org/10.1128/MCB.24.13.5914-5922.2004
Title: Essential roles of receptor-interacting protein and TRAF2 in oxidative stress-induced cell death
Authors: Shen, H.-M. 
Lin, Y.
Choksi, S.
Tran, J.
Jin, T.
Chang, L.
Karin, M.
Zhang, J.
Liu, Z.-G.
Issue Date: Jul-2004
Citation: Shen, H.-M., Lin, Y., Choksi, S., Tran, J., Jin, T., Chang, L., Karin, M., Zhang, J., Liu, Z.-G. (2004-07). Essential roles of receptor-interacting protein and TRAF2 in oxidative stress-induced cell death. Molecular and Cellular Biology 24 (13) : 5914-5922. ScholarBank@NUS Repository. https://doi.org/10.1128/MCB.24.13.5914-5922.2004
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 H2O 2 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 H 2O2. 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.
Source Title: Molecular and Cellular Biology
URI: http://scholarbank.nus.edu.sg/handle/10635/113465
ISSN: 02707306
DOI: 10.1128/MCB.24.13.5914-5922.2004
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