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,¶,1
Departments of
Physiology and
* Community Occupational and Family Medicine, Yong Loo Lin School of Medicine, and
¶ NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore
1Correspondence: Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Bldg. MD9, Level 3, Singapore 117597, Singapore. E-mail: phssp{at}nus.edu.sg
Tumor necrosis factor (TNF) superfamily is a group of cytokines with important functions in immunity, inflammation, differentiation, control of cell proliferation, and apoptosis. TNF
is the founding member of the 19 different proteins that have so far been identified within this family. TNF family members exert their biological effects through the TNF receptor (TNFR) superfamily of cell surface receptors that share a stretch of 
80 amino acids within their cytoplasmic region, the death domain (DD), critical for recruiting the death machinery. Work over the last decade has unraveled critical signaling networks involved in TNFR-induced cell death, specifically using the constitutively expressed TNFR1 as a prototype. Of particular interest is the intermediary role of intracellular reactive oxygen species (ROS) in signal transduction after ligation of the TNFR1. With the increasing understanding of the of death receptor signaling pathways, the exact role of ROS in TNF-induced execution is now believed to be far more complicated than originally thought. Recently, some important discoveries have underscored the critical role of ROS in TNF signaling, notably in TNF-mediated activation of nuclear factor-
B (NF-B) and c-Jun N-terminal kinase (c-Jun NH2-terminal kinase, JNK), as well as in cell death (apoptotic and necrotic) pathways. Here we attempt to review the existing knowledge on the involvement of ROS in death receptor signaling using TNF-TNFR1 as the model system, specifically addressing the involvement of intracellular ROS in TNF-induced cell death and in TNF-induced activation of NF-B and JNK and their crosstalk.—Shen, H-M., Pervaiz, S. TNF receptor superfamily-induced cell death: redox-dependent execution.
Key Words: oxidative stress • reactive oxygen species • death receptor • TRAF
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