Qin S, Ding J, Kurosaki T, Yamamura H
Department of Biochemistry, Kobe University School of Medicine, Japan.
FEBS Lett. 1998 May 1;427(1):139-43. doi: 10.1016/s0014-5793(98)00383-4.
Syk deficiency significantly enhanced ceramide-induced apoptosis. Ectopic expression of wild-type or kinase-inactive Syk rendered Syk-negative cells resistant to ceramide-induced apoptosis. Furthermore, ceramide could not activate Syk, indicating that Syk protected DT40 cells from ceramide-induced apoptosis, via a mechanism independent of its activity. In addition, a deficiency in Lyn also resulted in the cells becoming susceptible to ceramide-induced apoptosis. However, no difference of Ara-C-induced apoptosis between wild-type and mutant cells was observed. c-Jun N-terminal kinases appeared not to be important in mediating the enhanced apoptosis, as they were still activated in mutant cells following ceramide treatment.
