Fas-induced programmed cell death is mediated by a Ras-regulated O2- synthesis.

摘要: Fas induces apoptosis in lymphocytes via a poorly defined intracellular signalling cascade. Previously, we have demonstrated the involvement and significance of cascade from receptor sphingomyelinases ceramide to Ras Fas-induced apoptosis. Here demonstrate rapid transient synthesis reactive oxygen intermediates (ROI) activation after Fas. Genetic inhibition by transfection transdominant inhibitory N17Ras blocked Fas-mediated ROI programmed cell death. Likewise, antioxidants N-acetyl-cysteine N-t-butyl-phenylnitrone abolished death, pointing an important role for Ras-triggered