Abstract
Nuclear factor-κB (NF-κB) and c-Jun NH2-terminal kinase (JNK) are activated simultaneously under a variety of stress conditions. They also share several common signaling pathways for their activation in response to cytokines or growth factors. Recent studies, however, demonstrated a new form of interplay between these two allies. Inhibition of NF-κB by ikkβ or rela gene deficiency sensitizes stress responses through enhanced or prolonged activation of JNK. Conversely, sustained activation of NF-κB inhibits cytokine-induced JNK activation. The mechanisms of how NF-κB and JNK become rivals for each other are under extensive debate.
| Original language | English |
|---|---|
| Pages (from-to) | 1902-1905 |
| Number of pages | 4 |
| Journal | Cancer Research |
| Volume | 64 |
| Issue number | 6 |
| DOIs | |
| State | Published - Mar 15 2004 |
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