作者: Shang-Ze Li , Hui-Hui Zhang , Jun-Bo Liang , Yang Song , Bing-Xue Jin
DOI: 10.1016/J.BBAMCR.2014.03.028
关键词:
摘要: Stringent negative regulation of the transcription factor NF-κB is essential for maintaining cellular stress responses and homeostasis. However, tight mechanisms IKKβ are still not clear. Here, we reported that nemo-like kinase (NLK) a suppressor tumor necrosis (TNFα)-induced signaling by inhibiting phosphorylation IKKβ. Overexpression NLK largely blocked TNFα-induced activation, p65 nuclear localization IκBα degradation; whereas genetic inactivation showed opposing results. Mechanistically, identified interacted with IκB (IKK)-associated complex, which in turn inhibited assembly TAK1/IKKβ thereby, diminished phosphorylation. Our results indicate functions as pivotal regulator activation via disrupting interaction TAK1