One Man's JNK is a Scientist's Treasure

© 2003 Nature Publishing Group  CROSS TALKING PATHWAYS: Schematic depicting the TNF-R1-induced pathways modulating apoptosis. Blocking the NF-kB-dependent pathway leads to sustained JNK activation and apoptosis. Conversely, blocking the TNF-a induced JNK pathway promotes cell survival. JNK may induce death by triggering mitochondrial events, either directly or indirectly, but its targets remain unknown. (From G. Franzoso et al., Cell Death Differ, 10:13-15. doi: 10.1038/sj.cdd4401154)

Mark Greener
Dec 1, 2003
© 2003 Nature Publishing Group
 CROSS TALKING PATHWAYS: Schematic depicting the TNF-R1-induced pathways modulating apoptosis. Blocking the NF-kB-dependent pathway leads to sustained JNK activation and apoptosis. Conversely, blocking the TNF-a induced JNK pathway promotes cell survival. JNK may induce death by triggering mitochondrial events, either directly or indirectly, but its targets remain unknown. (From G. Franzoso et al., Cell Death Differ, 10:13-15. doi: 10.1038/sj.cdd4401154)

Molecular pathways that influence cellular life-and-death decisions increasingly fall under the scientific spotlight. In 1996, researchers discovered that NF-kB is anti-apoptotic, which led to the transcription factor becoming the subject of intense research. More recently, the intracellular signaling enzyme c-jun N-terminal kinase (JNK) emerged as a key promoter of cell suicide. Research into the seemingly opposing roles of these proteins' respective pathways may lead to treatments for several diseases, including organ failure, cancer, and rheumatoid arthritis.

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