IκBα is an inhibitor of the NFκB complex and inactivates the NFκB by trapping it in the cytoplasm. Phosphorylation of serine residues on the IκB protein by IκB kinases (IKKs) marks it for destruction via the ubiquitination pathway, thereby allowing the activation of the NFκB complex. Synthetic glucocorticoid such as dexamethasone display anti-inflammatory effects by inducing the increased synthesis of the IκB protein thereby inhibiting the activity of the NFκB complex. Overexpression of the IκBα gene in fibroblasts leads to inhibition of production of IL-6, TNF receptor, MMP-1, MMP-3 and MMP-13.
Science (New York, N.Y.), 270(5234), 286-290 (1995-10-13)
Glucocorticoids are among the most potent anti-inflammatory and immunosuppressive agents. They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function, but the mechanism underlying this activity has been unclear. Here it is
The Journal of rheumatology, 34(3), 523-533 (2007-02-14)
To investigate the role of the transcription factor nuclear factor-kB (NF-kappaB) in promoting inflammatory and destructive responses in human osteoarthritis (OA) synovial fibroblasts, by assessing the effect of NF-kappaB blockade on the production of cytokines and destructive enzymes. Infection with
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