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

Open access
Li, Qiutang, Estepa, Gabriela, Memet, Sylvie, Israel, Alain, Verma, Inder M.·2000·Genes & Development

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 from IKK1−/−/IKK2−/−embryos did not respond to NF-κB inducers. Upon crossing with κB–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.

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Metadata

Authors
Li, Q., Estepa, G., Memet, S., Israel, A., & Verma, I. M.
Venue
Genes & Development
Published
2000-07-15
Volume
14
Issue
14
Pages
1729-1733
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2134511627
Cited by
203
References
4
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: Complete lack of NF-κB activity in IKK1 and IKK2 double-deficient mice: additional defect in neurulation. https://app.cochat.ai/papers/10.1101/gad.14.14.1729
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Li, Q., Estepa, G., Memet, S., Israel, A., & Verma, I. M. (2000). Complete lack of NF-κB activity in IKK1 and IKK2 double-deficient mice: additional defect in neurulation. Genes & Development. https://doi.org/10.1101/gad.14.14.1729

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