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Adriamycin activated caspase\u20103 before the rise in JNK activity, while the response to cisplatin occurs hours after JNK activation. The increase in JNK activity was necessary for cisplatin\u2010mediated apoptosis but it was dispensable for adriamycin\u2010induced cell death. Cells derived from c\u2010jun knock out mice were more resistant to cisplatin cell death than normal cells, but no difference was observed in response to adriamycin. Activation of JNK and cell death by cisplatin is mediated by the MEKK1\/SEK1 cascade, since expression of dominant negative expression vectors of these kinases blocked both processes. p38 was also activated by cisplatin with similar kinetics as JNK. AP\u20101 complexes were activated by cisplatin including mainly c\u2010jun\/ATF\u20102 heterodimers suggesting that AP\u20101\u2010dependent transcription partially mediated cisplatin\u2010induced apoptosis.<\/jats:p>","DOI":"10.1016\/s0014-5793(99)00690-0","type":"journal-article","created":{"date-parts":[[2002,7,25]],"date-time":"2002-07-25T17:52:28Z","timestamp":1027619548000},"page":"151-158","source":"Crossref","is-referenced-by-count":84,"title":["Lack of c\u2010Jun activity increases survival to 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