Zhang Yadong, Chen Fei
Institute for Nutritional Sciences, Chinese Academy of Sciences, Shanghai, P. R. China.
Cancer Res. 2004 Mar 15;64(6):1902-5. doi: 10.1158/0008-5472.can-03-3361.
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.
核因子-κB(NF-κB)和c-Jun氨基末端激酶(JNK)在多种应激条件下会同时被激活。它们在响应细胞因子或生长因子时的激活也共享一些常见的信号通路。然而,最近的研究表明这两个“盟友”之间存在一种新的相互作用形式。通过ikkβ或relA基因缺陷抑制NF-κB会通过增强或延长JNK的激活来使应激反应敏感化。相反,NF-κB的持续激活会抑制细胞因子诱导的JNK激活。NF-κB和JNK如何成为彼此对手的机制正在广泛讨论中。