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.
In this issue's Hot Papers, Anning Lin and others at Chicago's Ben May Institute for Cancer Research demonstrated that genes controlled by NF-kB inhibit JNK's pro-apoptotic activity.1 Another group at Ben May led by Guido Franzoso proposed that a protein, gadd45b, seems to downregulate JNK's pro-apoptotic activity.2 Two more Hot Papers from groups at San Diego-based Celgene3 and the University of San Diego4 showed that a synthetic JNK inhibitor, SP600125, downregulates expression of inflammatory ...
