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Arresting NF-kB by B-arrestin2.

Authors
Chen-F
Source
Cell Death Differ 2004 Nov; 11(11):1155-1156
NIOSHTIC No.
20025860
Abstract
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.
Keywords
Genes; Cell-migration; Cell-growth; Physiological-effects; Physiological-factors; Diseases; Disease-prevention; Genetics; Genetic-disorders; Genotoxic-effects
Contact
Pathology and Physiology Research Branch, The Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA
CODEN
CDDIEK
Publication Date
20041101
Document Type
Journal Article
Email Address
LDF3@cdc.gov
Fiscal Year
2005
NTIS Accession No.
NTIS Price
Issue of Publication
11
ISSN
1350-9047
NIOSH Division
HELD
Source Name
Cell Death and Differentiation
State
WV
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