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

Cathy Tournier, Patricia Hess, Derek D. Yang, Jie Xu, Tod K. Turner, Anjaruwee Nimnual, Dafna Bar-Sagi, Stephen N. Jones, Richard A. Flavell, Roger J. Davis

Research output: Contribution to journalArticlepeer-review

1481 Scopus citations

Abstract

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 ink 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.

Original languageEnglish (US)
Pages (from-to)870-874
Number of pages5
JournalScience
Volume288
Issue number5467
DOIs
StatePublished - May 5 2000

All Science Journal Classification (ASJC) codes

  • General

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