Overview:

IκBα is an inhibitor of the NFκB complex and inactivates the NFκB by trapping it in the cytoplasm (1). 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 (2).

Gene Aliases:

NFKBIA, MAD-3, NFKBI

Genbank Number:

NM_020529

References:

1. Auphan, N. Et al: Immunosuppression by glucocorticoids: inhibition of NF-kappa-B activity through induction of I-kappa-B synthesis. Science 270: 286-290, 1995.

2. Bondeson, J. Et al: Adenoviral gene transfer of the endogenous inhibitor IkappaBalpha into human osteoarthritis synovial fibroblasts demonstrates that several matrix metalloproteinases and aggrecanases are nuclear factor-kappaB-dependent. J Rheumatol. 2007 Mar;34(3):523-33.