NF-κB is required for UV-induced JNK activation via induction of PKCδ

被引:94
|
作者
Liu, J
Yang, D
Minemoto, Y
Leitges, M
Rosner, MR
Lin, A
机构
[1] Univ Chicago, Ben May Inst Canc Res, Chicago, IL 60637 USA
[2] Max Planck Inst Expt Endocrinol, Hannover, Germany
关键词
D O I
10.1016/j.molcel.2005.12.020
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
Ultraviolet (UV) exerts its biological activities by activating downstream effectors, including NF-kappa B, JNK, and caspases. Activation of JNK is required for UV-induced apoptosis. It is unknown whether any crosstalk occurs between NF-kappa B and JNK in response to UV and, if so, how it affects UV killing. Here we report that NF-kappa B promotes UV-induced JNK activation, thereby contributing to UV-induced apoptosis. UV-induced JNK activation is impaired in ReIA/NF-kappa B null murine embryonic fibroblasts. In resting cells, the preexisting nuclear ReIA has already been recruited to PKC delta promoter and is essential for its expression. UV-induced rapid and robust activation of JNK requires PKC delta, which augments JNK phosphorylation-activation by its upstream kinases. The ReIA/NF-kappa B-PKC delta-JNK pathway is critical for UV-induced apoptosis, as it induces the immediate expression of the proapoptotic Fas ligand. Thus, our results demonstrate that ReIA/NF-kappa B via PKC delta positively regulates UV-induced JNK activation and provide a mechanism by which NF-kappa B promotes UV-induced apoptosis.
引用
收藏
页码:467 / 480
页数:14
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