JunD mediates survival signaling by the JNK signal transduction pathway
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UMass Chan Affiliations
Howard Hughes Medical Institute and Program in Molecular MedicineGraduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
2003-06-25Keywords
Animals; Apoptosis; Cell Line; Cell Survival; DNA Fragmentation; Enzyme Activation; Fibroblasts; Gene Expression Regulation; Genes, Reporter; Mice; Mitogen-Activated Protein Kinases; Models, Biological; NF-kappa B; Protein Isoforms; Proto-Oncogene Proteins c-jun; *Signal Transduction; Time Factors; Transcription, Genetic; Tumor Necrosis Factor-alphaLife Sciences
Medicine and Health Sciences
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Show full item recordAbstract
The c-Jun NH(2)-terminal kinase (JNK) can cause cell death by activating the mitochondrial apoptosis pathway. However, JNK is also capable of signaling cell survival. The mechanism that accounts for the dual role of JNK in apoptosis and survival signaling has not been established. Here we demonstrate that JNK-stimulated survival signaling can be mediated by JunD. The JNK/JunD pathway can collaborate with NF-kappaB to increase antiapoptotic gene expression. This observation accounts for the ability of JNK to cause either survival or apoptosis in different cellular contexts. Furthermore, these data illustrate the general principal that signal transduction pathway integration is critical for the ability of cells to mount an appropriate biological response to a specific challenge.Source
Mol Cell. 2003 Jun;11(6):1479-89.
DOI
10.1016/S1097-2765(03)00203-XPermanent Link to this Item
http://hdl.handle.net/20.500.14038/33986PubMed ID
12820962Related Resources
ae974a485f413a2113503eed53cd6c53
10.1016/S1097-2765(03)00203-X