Figure 11.

Regulation of NFκB activity by c-jun. Cisplatin activates both JNK and NFκB-dependent transcription by a common kinase, MEKK1. In normal cells when JNK is activated, c-jun is phosphorylated, and translocation of p50/p65 active complexes takes place. C-jun, on one hand, activates FasL transcription and inhibits NFκB-dependent transcription, inhibiting the expression of genes involved in cell survival such as MIAP3. In c-jun^−/− cells, the activation of p65-dependent transcription is no longer inhibited, and even if FasL expression can take place because of the NFκB site in the promoter, the transcription triggered by NFκB leads cells to survival by maintaining expression of MIAP3.