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Nuclear factor-kappa B.

Authors: P J, Barnes;

Nuclear factor-kappa B.

Abstract

Nuclear factor-kappa B (NF-kappa B) is a ubiquitous transcription factor that, by regulating the expression of multiple inflammatory and immune genes, plays a critical role in host defence and in chronic inflammatory diseases. It is a heterodimer, present in the cytoplasm in an inactive form complexed to an inhibitory protein, I kappa B. Many extracellular stimuli, including viruses, oxidants, inflammatory cytokines and immune stimuli, activate NF-kappa B. Once activated, it binds to recognition elements in the promoter regions of inflammatory and immune genes, such as proinflammatory cytokines, chemokines, inflammatory enzymes and adhesion molecules. Glucocorticoids inhibit activated NF-kappa B and this is likely to be important in the anti-inflammatory action of steroids. Novel inhibitors of NF-kappa B are now under development for treatment of inflammatory diseases such as asthma, rheumatoid arthritis and inflammatory bowel disease.

Keywords

Inflammation, Peptide Biosynthesis, Structure-Activity Relationship, Immunogenetics, NF-kappa B, Humans, Glucocorticoids

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Powered by OpenAIRE graph
Found an issue? Give us feedback
selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
305
Top 10%
Top 1%
Top 1%
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