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lüll The NF-kappaB-mediated control of the JNK cascade in the antagonism of programmed cell death in health and disease Papa S; Bubici C; Zazzeroni F; Pham CG; Kuntzen C; Knabb JR; Dean K; Franzoso GCell Death Differ 2006[May]; 13 (5): 712-29NF-kappaB/Rel transcription factors have recently emerged as crucial regulators of cell survival. Activation of NF-kappaB antagonizes programmed cell death (PCD) induced by tumor necrosis factor-receptors (TNF-Rs) and several other triggers. This prosurvival activity of NF-kappaB participates in a wide range of biological processes, including immunity, lymphopoiesis and development. It is also crucial for pathogenesis of various cancers, chronic inflammation and certain hereditary disorders. This participation of NF-kappaB in survival signaling often involves an antagonism of PCD triggered by TNF-R-family receptors, and is mediated through a suppression of the formation of reactive oxygen species (ROS) and a control of sustained activation of the Jun-N-terminal kinase (JNK) cascade. Effectors of this antagonistic activity of NF-kappaB on this ROS/JNK pathway have been recently identified. Indeed, further delineating the mechanisms by which NF-kappaB promotes cell survival might hold the key to developing new highly effective therapies for treatment of widespread human diseases.|*Apoptosis[MESH]|*Disease[MESH]|*Gene Expression Regulation[MESH]|*Health[MESH]|Animals[MESH]|Evolution, Molecular[MESH]|Humans[MESH]|JNK Mitogen-Activated Protein Kinases/*metabolism[MESH]|Models, Biological[MESH]|NF-kappa B/metabolism/*physiology[MESH]|Necrosis[MESH]|Neoplasms/*metabolism/pathology[MESH]|Reactive Oxygen Species/metabolism[MESH]|Receptors, Tumor Necrosis Factor/physiology[MESH]|Signal Transduction[MESH]|Tumor Necrosis Factor-alpha/pharmacology[MESH] |