Reactive oxygen species (ROS), troublemakers between nuclear factor-κB (NF-κB) and c-jun NH2-terminal kinase (JNK)

Nuclear factor-kappaB (NF-kappaB) 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-kappaB by ikkbeta or rela gene deficiency sensitizes stress responses through enhanced or prolonged activation of JNK. Conversely, sustained activation of NF-kappaB inhibits cytokine-induced JNK activation. The mechanisms of how N-kappaB and JNK become rivals for each other are under extensive debate.