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Nck1/2 recruitment to tyrosine phosphorylated proteins promote IKK-dependent NF-κB activation and proinflammatory gene expression. Oxidative stress (H2O2, ischemia/reperfusion injury) promotes Nck1/2 recruitment through PECAM-1 phosphorylation. In disturbed flow, Nck1 recruitment to IRAK-1 promotes NF-κB activation through a pathway that may or may not involve PAK2.
