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Reactive Oxygen Species (ROS), Troublemakers between Nuclear Factor-κB (NF-κB) and c-Jun NH2-terminal Kinase (JNK)

  • Chinese Academy of Sciences

Research output: Contribution to journalReview articlepeer-review

163 Scopus citations

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 languageEnglish
Pages (from-to)1902-1905
Number of pages4
JournalCancer Research
Volume64
Issue number6
DOIs
StatePublished - Mar 15 2004

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