Answers are grounded in this paper and cite their sources.
Nuclear factor-kappaB (NF-kappaB) and c-Jun NH(2)-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 NF-kappaB and JNK become rivals for each other are under extensive debate.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2004) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: