The c-Jun N-terminal kinase (JNK) group of mitogen-activated protein kinase
s (MAPKs) is activated in mammalian cells by environmental stress, pro-Infl
ammatory cytokines, and mitogenic stimuli. Biochemical and genetic studies
demonstrate that JNK regulates the activities of many transcription factors
, and that the JNK pathway is required for the regulation of inflammatory r
esponses, cell proliferation, and apoptosis. The involvement of JNK in apop
totic cell death is particularly intriguing, and has been actively studied
in recent years. An improved understanding of JNK-mediated apoptotic signal
ing may provide novel strategies in prevention and treatment of cancers.