A body of evidence suggests that stress-induced sphingomyelin hydrolysis to the second
messenger ceramide initiates apoptosis in some cells. Although studies using lymphoblasts
from Niemann-Pick disease patients or acid sphingomyelinase (ASMase)-deficient mice
have provided genetic support for this hypothesis, these models have not been universally
accepted as definitive. Here, we show that mouse embryonic fibroblasts (MEFs) prepared
from asmase mice manifest cell autonomous defects in apoptosis in response to several …