| First Author | Yeh WC | Year | 1998 |
| Journal | Science | Volume | 279 |
| Issue | 5358 | Pages | 1954-8 |
| PubMed ID | 9506948 | Mgi Jnum | J:46527 |
| Mgi Id | MGI:1201276 | Doi | 10.1126/science.279.5358.1954 |
| Citation | Yeh WC, et al. (1998) FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis. Science 279(5358):1954-8 |
| abstractText | FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas), CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD- deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD- deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling. |
