Hepatic expression of S32A/S36A IκBα does not reduce postischemic liver injury

The data demonstrate that the pathway of NF-κB activation involving serine phosphorylation of IκBα is not the primary mechanism for induction of liver inflammation after ischemia/reperfusion and suggest that alternative pathways, such as tyrosine phosphorylation of IκBα, may be essential for the postischemic response in liver.