JunD mediates survival signaling by the JNK signal transduction pathway

被引:218
作者
Lamb, JA
Ventura, JJ
Hess, P
Flavell, RA
Davis, RJ [1 ]
机构
[1] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
[2] Univ Massachusetts, Sch Med, Program Mol Med, Dept Biochem & Mol Biol, Worcester, MA 01605 USA
[3] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA
[4] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA
关键词
D O I
10.1016/S1097-2765(03)00203-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The c-Jun NH2-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.
引用
收藏
页码:1479 / 1489
页数:11
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