| First Author | Zumbansen M | Year | 1997 |
| Journal | J Biol Chem | Volume | 272 |
| Issue | 16 | Pages | 10904-9 |
| PubMed ID | 9099747 | Mgi Jnum | J:39584 |
| Mgi Id | MGI:86938 | Doi | 10.1074/jbc.272.16.10904 |
| Citation | Zumbansen M, et al. (1997) Tumor necrosis factor alpha activates NF-kappaB in acid sphingomyelinase-deficient mouse embryonic fibroblasts. J Biol Chem 272(16):10904-9 |
| abstractText | Tumor necrosis factor alpha (TNF-alpha) is one of the most potent inducer of the nuclear transcription factor kappaB (NF-kappaB). Activation of NF-kappaB is initiated by phosphorylation of the inhibitory subunit of the IkappaB-alpha-NF-kappaB complex. This leads to the dissociation of the complex and degradation of IkappaB-alpha. NF-kappaB is translocated into the nucleus. The sphingomyelin pathway is thought to mediate the TNF-alpha-induced activation of NF-kappaB by its second messenger ceramide. We have used the recently established acid sphingomyelinase-deficient mouse line (asmase-/- mice) to evaluate the role of acid sphingomyelinase in the TNF-alpha-induced signal transduction pathway. Here we present experimental evidence that acid sphingomyelinase is not involved in the TNF-alpha-induced activation of NF-kappaB. TNF-alpha treatment induced the dissociation and degradation of IkappaB-alpha and the nuclear translocation of NF-kappaB in embryonic fibroblasts derived from asmase-/- and wild type mice indiscriminately. |
