IκBa inhibits activation of the NF-κB pathway activation by associating with the major NF-κB heterodimeric complex p50/p65 and preventing its translocation from the cytoplasm into the nucleus, where it acts a transcription factor for genes involved in inflammation, autoimmune response, cell proliferation, and apoptosis. Inhibition of NF-κB pathway activation by IκBα is controlled by its sequential serine-phosphorylation, ubiquitination and proteasomal degradation. This process itself can be inhibited by SUMOylation of IκBα, providing an additional regulatory step for the activation of the NF-κB pathway.
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