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Arresting NF-kB by B-arrestin2.
Cell Death Differ 2004 Nov; 11(11):1155-1156
Any activity without restriction can be dangerous for the proper function of an organism. The same is ture for NF-kB, a ubiquitous transcription factor governing the expression of genes involved in cell-to-cell communication, cell-to-cell interaction, cell migration, cell cycle, and cell growth regulation during both normal physiological conditions and pathological circumstances. A number of endogenous inhibitors that restrict the activation or activity of NF-kB have been identified recently, in addition to 1kB family proteins. The most remarkable regulatory mechanism of NF-kB activation is its association with the endogenous inhibitors the 1kB family proteins that retain it in the cytoplam. In response to extracellular signals, the inhibitory proteins are first phosphorylated through the activation of kinase cascades, such as 1kb kinase complexes (IKK), and then degraded in a ubiquitin-proteasome-dependent manner.
Genes; Cell-migration; Cell-growth; Physiological-effects; Physiological-factors; Diseases; Disease-prevention; Genetics; Genetic-disorders; Genotoxic-effects
Pathology and Physiology Research Branch, The Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA
Issue of Publication
Cell Death and Differentiation
Page last reviewed: September 2, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division