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

NF-kappa B activity is induced by cytokines, stress, and pathogens. IKK1 an d IKK2 are critical I kappa B kinases in NF-kappa B activation. In this stu dy mice lacking IKK1 and IKK2 died at E12. Additional defect in neurulation associated with enhanced apoptosis in the neuroepithelium was also observe d. MEF cells from IKK-/-/IKK2(-/-) embryos did not respond to NF-kappa B in ducers. Upon crossing with kappa B-lacZ transgenic mice, double-deficient e mbryos also lost lacZ transgene expression in vascular endothelial cells du ring development. Our data suggest that IKK1 and IKK2 are essential for NF- kappa B activation in vivo and have an important role in protecting neurons against excessive apoptosis during development.