Complete lack of NF-κB activity in IKK1 and IKK2 double-deficient mice: additional defect in neurulation

Abstract

NF-κB activity is induced by cytokines, stress, and pathogens. IKK1 and IKK2 are critical IκB kinases in NF-κB activation. In this study mice lacking IKK1 and IKK2 died at E12. Additional defect in neurulation associated with enhanced apoptosis in the neuroepithelium was also observed. MEF cells fromIKK1−/−/IKK2−/−embryos did not respond to NF-κB inducers. Upon crossing withκB–lacZ transgenic mice, double-deficient embryos also lost lacZ transgene expression in vascular endothelial cells during development. Our data suggest that IKK1 and IKK2 are essential for NF-κB activation in vivo and have an important role in protecting neurons against excessive apoptosis during development.