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Vol. 14, No. 14, pp. 1729-1733, July 15, 2000
B activity in IKK1 and IKK2 double-deficient mice: additional defect in neurulation
1 Laboratory of Genetics, The Salk Institute, La Jolla,
California 92037 USA; 2 Institut Pasteur, 715724 Paris, Cedex
15, France
NF-
B activity is induced by cytokines, stress, and pathogens.
IKK1 and IKK2 are critical IB kinases in NF-B 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 from
IKK1
//IKK2/
embryos did not respond to NF-B inducers. Upon crossing with B-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-B activation in vivo and have an important
role in protecting neurons against excessive apoptosis during development.
[Key Words:
IKK; NF-B; knockout; endothelium; apoptosis; NTD]
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