Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway
C Tournier, P Hess, DD Yang, J Xu, TK Turner… - Science, 2000 - science.org
C Tournier, P Hess, DD Yang, J Xu, TK Turner, A Nimnual, D Bar-Sagi, SN Jones, RA Flavell…
Science, 2000•science.orgThe 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 …
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 …
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 Jnkgenes 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.
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