Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway

UMMS Affiliation

Howard Hughes Medical Institute and Program in Molecular Medicine; Department of Biochemistry and Molecular Pharmacology; Department of Cell Biology

Publication Date


Document Type



Animals; *Apoptosis; Apoptotic Protease-Activating Factor 1; Caspase 3; Caspase 9; Caspases; Cell Count; Cell Division; Cells, Cultured; Cytochrome c Group; DNA Fragmentation; Enzyme Activation; Fibroblasts; Gene Targeting; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; Methyl Methanesulfonate; Mice; Mitochondria; Mitogen-Activated Protein Kinases; NF-kappa B; *Protein-Serine-Threonine Kinases; Proteins; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Tumor Suppressor Protein p53; Ultraviolet Rays


Life Sciences | Medicine and Health Sciences


The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.

DOI of Published Version



Science. 2000 May 5;288(5467):870-4.

Journal/Book/Conference Title

Science (New York, N.Y.)

Related Resources

Link to Article in PubMed

PubMed ID