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

被引:1520
|
作者
Tournier, C
Hess, P
Yang, DD
Xu, J
Turner, TK
Nimnual, A
Bar-Sagi, D
Jones, SN
Flavell, RA
Davis, RJ [1 ]
机构
[1] Univ Massachusetts, Sch Med, Dept Biochem & Mol Biol, Program Mol Med,Howard Hughes Med Inst, Worcester, MA 01605 USA
[2] Yale Univ, Sch Med, Immunobiol Sect, Howard Hughes Med Inst, New Haven, CT 06520 USA
[3] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01605 USA
[4] SUNY Stony Brook, Dept Mol Genet & Microbiol, Stony Brook, NY 11794 USA
关键词
D O I
10.1126/science.288.5467.870
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:870 / 874
页数:5
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