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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development.

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.[1]

References

  1. Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development. Yeh, W.C., Itie, A., Elia, A.J., Ng, M., Shu, H.B., Wakeham, A., Mirtsos, C., Suzuki, N., Bonnard, M., Goeddel, D.V., Mak, T.W. Immunity (2000) [Pubmed]
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