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

Jing Liu, Dan Yang, Yuzuru Minemoto, Michael Leitges, Marsha R. Rosner, Anning Lin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

89 Scopus citations


Ultraviolet (UV) exerts its biological activities by activating downstream effectors, including NF-κB, JNK, and caspases. Activation of JNK is required for UV-induced apoptosis. It is unknown whether any crosstalk occurs between NF-κB and JNK in response to UV and, if so, how it affects UV killing. Here we report that NF-κB promotes UV-induced JNK activation, thereby contributing to UV-induced apoptosis. UV-induced JNK activation is impaired in RelA/NF-κB null murine embryonic fibroblasts. In resting cells, the preexisting nuclear RelA has already been recruited to PKCδ promoter and is essential for its expression. UV-induced rapid and robust activation of JNK requires PKCδ, which augments JNK phosphorylation- activation by its upstream kinases. The RelA/NF-κB-PKCδ-JNK pathway is critical for UV-induced apoptosis, as it induces the immediate expression of the proapoptotic Fas ligand. Thus, our results demonstrate that RelA/NF-κB via PKCδ positively regulates UV-induced JNK activation and provide a mechanism by which NF-κB promotes UV-induced apoptosis.

Original languageEnglish (US)
Pages (from-to)467-480
Number of pages14
JournalMolecular cell
Issue number4
StatePublished - Feb 17 2006

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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