Journal ArticleDOI
Function and activation of NF-kappa B in the immune system.
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TLDR
The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, severe phase response, and radiation damage.Abstract:
NF-kappa B is a ubiquitous transcription factor. Nevertheless, its properties seem to be most extensively exploited in cells of the immune system. Among these properties are NF-kappa B's rapid posttranslational activation in response to many pathogenic signals, its direct participation in cytoplasmic/nuclear signaling, and its potency to activate transcription of a great variety of genes encoding immunologically relevant proteins. In vertebrates, five distinct DNA binding subunits are currently known which might extensively heterodimerize, thereby forming complexes with distinct transcriptional activity, DNA sequence specificity, and cell type- and cell stage-specific distribution. The activity of DNA binding NF-kappa B dimers is tightly controlled by accessory proteins called I kappa B subunits of which there are also five different species currently known in vertebrates. I kappa B proteins inhibit DNA binding and prevent nuclear uptake of NF-kappa B complexes. An exception is the Bcl-3 protein which in addition can function as a transcription activating subunit in th nucleus. Other I kappa B proteins are rather involved in terminating NF-kappa B's activity in the nucleus. The intracellular events that lead to the inactivation of I kappa B, i.e. the activation of NF-kappa B, are complex. They involve phosphorylation and proteolytic reactions and seem to be controlled by the cells' redox status. Interference with the activation or activity of NF-kappa B may be beneficial in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, acute phase response, and radiation damage. The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes.read more
Citations
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Journal ArticleDOI
A New Function for the C-terminal Zinc Finger of the Glucocorticoid Receptor REPRESSION OF RelA TRANSACTIVATION
TL;DR: These results demonstrate that the inhibition of NF-κB by glucocorticoids involves two critical amino acids in the C-terminal zinc finger of the GR, and suggest that the mechanisms for GR-mediated repression of NF -κB and AP-1 are different.
Journal ArticleDOI
Inflammatory cytokines overcome age-related defects in CD4 T cell responses in vivo
TL;DR: It is suggested that induction of inflammatory cytokines via adjuvants, or the use of an adjuvant such as CFA that induces these cytokines, markedly enhanced responses of these aged CD4 T cells, so that they proliferated and produced IL-2 similar to young cells.
Journal ArticleDOI
Differential effects of glucose and alcohol on reactive oxygen species generation and intranuclear nuclear factor-κB in mononuclear cells
Sandeep Dhindsa,Devjit Tripathy,Priya Mohanty,Husam Ghanim,Tufail Syed,Ahmad Aljada,Paresh Dandona +6 more
TL;DR: It is concluded that 75 g oral glucose increases NF-kappaB binding activity in MNCs, and while 75 g glucose (300 calories) induces an increase in ROS generation and intranuclear NF- kappaB, equicaloric amounts of alcohol did not produce these effects.
Journal ArticleDOI
INHIBITION OF TNF-α AND IL-6 PRODUCTION BY AUCUBIN THROUGH BLOCKADE OF NF-κB ACTIVATION IN RBL-2H3 MAST CELLS
Hyun-Ja Jeong,Hyun-Na Koo,Ho-Jeong Na,Mi-Sun Kim,Seung-Heon Hong,Jung-Woo Eom,Kyung-Suk Kim,Tae-Yong Shin,Hyung-Min Kim +8 more
TL;DR: Results suggest that aucubin is a specific inhibitor of NF-κB activation in mast cells, which might explain its beneficial effect in the treatment of chronic allergic inflammatory diseases.
Journal ArticleDOI
Cellular Enrichment with Polyunsaturated Fatty Acids Induces an Oxidative Stress and Activates the Transcription Factors AP1 and NFκB
TL;DR: The results indicate that the accumulation of PUFA from (n-6) and ( n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.
References
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Book
Free radicals in biology and medicine
TL;DR: 1. Oxygen is a toxic gas - an introduction to oxygen toxicity and reactive species, and the chemistry of free radicals and related 'reactive species'
Journal ArticleDOI
Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1.
TL;DR: It is shown that micromolar concentrations of H2O2 can induce the expression and replication of HIV‐1 in a human T cell line and suggests that diverse agents thought to activate NF‐kappa B by distinct intracellular pathways might all act through a common mechanism involving the synthesis of ROI.
Journal ArticleDOI
Multiple nuclear factors interact with the immunoglobulin enhancer sequences.
Ranjan Sen,David Baltimore +1 more
TL;DR: In this paper, an electrophoretic mobility shift assay with end-labeled DNA fragments was used to characterize proteins that bind to the immunoglobulin (Ig) heavy chain and the kappa light chain enhancers.
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The mechanism of action of cyclosporin A and FK506
TL;DR: Recent findings that indicate CsA and FK506 operate as prodrugs are reviewed: they bind endogenous intracellular receptors, the immunophilins, and the resulting complex targets the protein phosphatase, calcineurin, to exert the immunosuppressive effect.
Journal ArticleDOI
An inducible transcription factor activates expression of human immunodeficiency virus in T cells
Gary J. Nabel,David Baltimore +1 more
TL;DR: Activation of T cells, which increases HIV expression up to 50-fold, correlated with induction of a DNA binding protein indistinguishable from a recognized transcription factor, called NF-κB, with binding sites in the viral enhancer.