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- W1967482006 abstract "We report here that stress stimuli such as γ-irradiation or the anticancer drug doxorubicin activate expression of the death-inducing ligands (DILs) CD95-L, TNF-α and TRAIL. Apoptosis induced by γ-irradiation or doxorubicin engages a FADD- and caspase-dependent apoptosis pathway which is inhibited by dominant negative FADD or the caspase inhibitor zVAD. zVAD did not prevent activity of JNK/SAPKs in response to doxorubicin suggesting that JNK/SAPK activity is independent of death receptor triggering during cellular stress-induced apoptosis. In addition, JNK/SAPKs remained activated by doxorubicin in resistant cell lines in which cleavage of caspases and apoptosis was not observed. These data uncouple JNK/SAPK activation and apoptosis signaling and indicate that cellular stress-induced apoptosis involves signaling via DILs which is paralleled by activation of JNK/SAPKs. Activation of these kinases may contribute e.g., to the expression of molecules involved in apoptosis but is not sufficient for induction of the apoptosis program following cellular stress. Int. J. Cancer 80:417–424, 1999. © 1999 Wiley-Liss, Inc." @default.
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- W1967482006 date "1999-01-29" @default.
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- W1967482006 title "JNK/SAPK activity is not sufficient for anticancer therapy-induced apoptosis involving CD95-L, TRAIL and TNF-?" @default.
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- W1967482006 doi "https://doi.org/10.1002/(sici)1097-0215(19990129)80:3<417::aid-ijc14>3.0.co;2-b" @default.
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