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The mechanism underlying sustained activation of NF-κB signaling associated with MIC-1 in intestinal epithelial cells infected with EPEC. EPEC infection can trigger prolonged NF-κB activation. Although the bacteria can regulate transient NF-κB activation and cytokine production via a type III secretion system during the early infection period, it extends p65 activation in a MIC-1-linked signaling pathway, which contributes to epithelial survival from bacteria-induced apoptotic death.
