| First Author | Tanaka M | Year | 1999 |
| Journal | Immunity | Volume | 10 |
| Issue | 4 | Pages | 421-9 |
| PubMed ID | 10229185 | Mgi Jnum | J:55680 |
| Mgi Id | MGI:1339763 | Doi | 10.1016/s1074-7613(00)80042-4 |
| Citation | Tanaka M, et al. (1999) Embryonic lethality, liver degeneration, and impaired NF-kappa B activation in IKK-beta-deficient mice. Immunity 10(4):421-9 |
| abstractText | 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. |
