Figure 1

Hypoxia activates NFκB signalling via inhibitor of κB kinase. Under conditions of hypoxia, the hydroxylase-mediated repression of inhibitor of κB kinase (IKK) beta is suppressed – leading to enhanced IKKβ activity, enhanced IκBα phosphorylation and degradation as well as increased p65 NFκB activity. Factor-inhibiting hypoxia inducible factor inhibition by hypoxia or pharmacological inhibition reduces IκBα asparaginyl hydroxylation but does not appear to affect IκBα degradation. COX-2, cyclooxygenase 2; ICAM-1, intracellular adhesion molecule 1; iNOS, inducible nitric oxide synthase; RANTES, regulated upon activation normal T-cell expressed and secreted; PHD-1, prolyl hydroxylase 1; VCAM-1, vascular cell adhesion molecule 1.