The NF-kappaB-mediated control of the JNK cascade in the antagonism of programmed cell death in health and disease
| Autor: | Francesca Zazzeroni, Christian Kuntzen, Can G. Pham, Salvatore Papa, Concetta Bubici, Guido Franzoso, Kathryn Dean, James R. Knabb |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Programmed cell death
Apoptosis Biology Models Biological Receptors Tumor Necrosis Factor Evolution Molecular chemistry.chemical_compound Necrosis Neoplasms Animals Humans Disease Lymphopoiesis Molecular Biology Transcription factor Tumor Necrosis Factor-alpha JNK Mitogen-Activated Protein Kinases NF-kappa B NF-κB Cell Biology Cell biology chemistry Gene Expression Regulation Health JNK cascade Tumor necrosis factor alpha Signal transduction Reactive Oxygen Species Signal Transduction |
| Zdroj: | Cell death and differentiation. 13(5) |
| ISSN: | 1350-9047 |
| Popis: | NF-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. |
| Databáze: | OpenAIRE |
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