Work

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

Year: 2000

Type: preprint

Abstract: NF-kappaB activity is induced by cytokines, stress, and pathogens. IKK1 and IKK2 are critical IkappaB kinases in NF-kappaB 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-kappaB inducers. Upon crossing with kappaB-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-kappaB activation in vivo and have an important role in protecting neurons against excessive apoptosis during development.

Source: Genes & Development

DOI: 10.1101/gad.14.14.1729

Authors: Qiutang Li, Gabriela Estepa, Sylvie Memet, Alain Israel, Inder M. Verma

Institutions: Salk Institute for Biological Studies, Institut Pasteur

Language: English

Topic: NF-κB Signaling Pathways

Subfield: Cancer Research

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: diamond

Funders: March of Dimes Foundation, Wayne and Gladys Valley Foundation, National Institutes of Health