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Embryonic lethality, liver degeneration, and impaired NF-kappa B activation in IKK-beta-deficient mice.

IkappaB kinase-alpha and -beta (IKK-alpha and IKK-beta), the catalytic subunits of the IKK complex, phosphorylate IkappaB proteins on specific serine residues, thus targeting IkappaB for degradation and activating the transcription factor NF-kappaB. To elucidate the in vivo function of IKK-beta, we generated IKK-beta-deficient mice. The homozygous mouse embryo dies at approximately 14.5 days of gestation due to liver degeneration and apoptosis. IKK-beta-deficient embryonic fibroblasts have both reduced basal NF-kappaB activity and impaired cytokine-induced NF-kappaB activation. Similarly, basal and cytokine-inducible kinase activities of the IKK complex are greatly reduced in IKK-beta-deficient cells. These results indicate that IKK-beta is crucial for liver development and regulation of NF-kappaB activity and that IKK-alpha can only partially compensate for the loss of IKK-beta.

Pubmed ID: 10229185


  • Tanaka M
  • Fuentes ME
  • Yamaguchi K
  • Durnin MH
  • Dalrymple SA
  • Hardy KL
  • Goeddel DV



Publication Data

April 20, 1999

Associated Grants


Mesh Terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Cell Line
  • Crosses, Genetic
  • Enzyme Activation
  • Female
  • Fetal Death
  • Humans
  • I-kappa B Kinase
  • Interleukin-6
  • JNK Mitogen-Activated Protein Kinases
  • Liver
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogen-Activated Protein Kinases
  • NF-kappa B
  • Protein-Serine-Threonine Kinases
  • Transfection
  • Tumor Necrosis Factor-alpha