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Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, Pennsylvania
Nuclear factor kappa B (NF-KB) is an ubiquitous rapid response transcription factor in cells involved in imune and inflammatory reactions, and exerts its effect by expressing cytokines, chemokines, cell adhesion moecules, growth factors, and immunoreceptors. In this manner, NF-KB contributes to immunologically medated diseases such as allograft rejection, rheumatoid arthritis, and bronchial asthma. The prototypic induible form of NF-KB is a heterodimer composed of NF-kB1 and RelA, which both belong to the NF-KB/Rel family of proteins. Inactive NF-KB is present in the cytoplasm complexed with an inhibitory protein, IKB. NF-KB is activated by a number of incoming signals from the cell surface. Released from IKB inhibition, NF-KB translcates into the nucleus and binds to the KB motif of the target gene. The NF-KB activation process can be inhiited by pharmacologic agents at each activation step. Glucocorticoids inhibit NF-KB by directly associating with NF-KB or by upregulating IKB expression. Cyclsporine and tacrolimus prevent NF-KB activation by ihibiting the action of calcineurin, a phosphatase that indirectly induces IKB degradation. Deoxyspergualin ihibits NF-KB by blocking its nuclear translocation. Apirin and salicylates inhibit upstream events inducing IKB phosphorylation. Tepoxalin and antioxidants ihibit NF-KB activation by influencing the redox state of the cell. Further research is required to develop more specific inhibitors to treat diseases mediated by NF-KB.
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