| First Author | Yeh WC | Year | 2000 |
| Journal | Immunity | Volume | 12 |
| Issue | 6 | Pages | 633-42 |
| PubMed ID | 10894163 | Mgi Jnum | J:63049 |
| Mgi Id | MGI:1860369 | Doi | 10.1016/s1074-7613(00)80214-9 |
| Citation | Yeh WC, et al. (2000) Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development. Immunity 12(6):633-42 |
| abstractText | Casper (c-FLIP) associates with FADD and caspase-8 in signaling complexes downstream of death receptors like Fas. We generated Casper-deficient mice and cells and noted a duality in the physiological functions of this molecule. casper-/- embryos do not survive past day 10.5 of embryogenesis and exhibit impaired heart development. This phenotype is reminiscent of that reported for FADD-/- and caspase-8-/- embryos. However, unlike FADD-/- and caspase-8-/- cells, casper-/- embryonic fibroblasts are highly sensitive to FasL- or TNF-induced apoptosis and show rapid induction of caspase activities. NF-kappaB and JNK/SAPK activation is intact in TNF-stimulated casper-/- cells. These results suggest that Casper has two distinct roles: to cooperate with FADD and caspase-8 during embryonic development and to mediate cytoprotection against death factor-induced apoptosis. |
