
The transcription factor NF-kappa B is a key regulator of genes involved in responses to infection, inflammation and stress. It was first identified as a protein with ADN-binding activity specific for the 10-base-pair kappa B site in the immunoglobulin k light-chain enhancer of B lymphocytes.NF-kappa B is normally present in the cell cytoplasm bound to an inhibitory I kappa B protein. The nuclear localization signal (NLS) in NF-kappa B is a short amino acid signal sequence involved in nuclear transport. Inducers of NF-kappa activation trigger dissociation and degradation of I kappa B from the NF-kappa B complex. This allows NF-kappa B to translocate to the nucleus and bind to kappa B DNA sites. Repression of NF-kappa B dependent gene expression is one of the major elements of immunosuppression by glucocorticoids. FUTURES PROSPECTS AND PROJECTS: Endothelial cells at sites of inflammatory responses express a variety of genes that are under the control of nuclear factor NF-kappa B. This transcriptional factor with its inhibitors may be linked in an autoregulatory system that can be activated by multiple signals relevant to vascular pathophysiology. NF-kappa B is therefore an obvious target for new types of anti-inflammatory treatment.
Inflammation, Gene Expression Regulation, Transcription, Genetic, NF-kappa B, Humans, Endothelium, Infections, Stress, Psychological, Translocation, Genetic, Signal Transduction
Inflammation, Gene Expression Regulation, Transcription, Genetic, NF-kappa B, Humans, Endothelium, Infections, Stress, Psychological, Translocation, Genetic, Signal Transduction
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