| First Author | Varfolomeev EE | Year | 1998 |
| Journal | Immunity | Volume | 9 |
| Issue | 2 | Pages | 267-76 |
| PubMed ID | 9729047 | Mgi Jnum | J:49459 |
| Mgi Id | MGI:1277504 | Doi | 10.1016/s1074-7613(00)80609-3 |
| Citation | Varfolomeev EE, et al. (1998) Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally. Immunity 9(2):267-76 |
| abstractText | Homozygous targeted disruption of the mouse Caspase 8 (Casp8) gene was found to be lethal in utero. The Caspase 8 null embryos exhibited impaired heart muscle development and congested accumulation of erythrocytes. Recovery of hematopoietic colony-forming cells from the embryos was very low. In fibroblast strains derived from these embryos, the TNF receptors, Fas/Apo1, and DR3 were able to activate the Jun N-terminal kinase and to trigger IkappaB alpha phosphorylation and degradation. They failed, however, to induce cell death, while doing so effectively in wild-type fibroblasts. These findings indicate that Caspase 8 plays a necessary and nonredundant role in death induction by several receptors of the TNF/NGF family and serves a vital role in embryonal development. |
