期刊
CELL DEATH AND DIFFERENTIATION
卷 13, 期 5, 页码 712-729出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401865
关键词
NF-kappa B; JNK; ROS; apoptosis; necrosis; programmed cell death
资金
- NCI NIH HHS [R01-CA84040, R01-CA098583] Funding Source: Medline
NF-kappa B/Rel transcription factors have recently emerged as crucial regulators of cell survival. Activation of NF-kappa B antagonizes programmed cell death ( PCD) induced by tumor necrosis factor- receptors ( TNF- Rs) and several other triggers. This prosurvival activity of NF-kappa B 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-kappa B 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-kappa B on this ROS/ JNK pathway have been recently identified. Indeed, further delineating the mechanisms by which NF-kappa B promotes cell survival might hold the key to developing new highly effective therapies for treatment of widespread human diseases.
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