作者
Tao Zhang,Daichao Xu,Elijah Trefts,Mingming Lv,Hiroyuki Inuzuka,Guobin Song,Min Liu,Jianlin Lu,Jianping Liu,Chen Chu,Min Wang,Huibing Wang,Huyan Meng,Hui Liu,Yuan Zhuang,Xingxing Xie,Fabin Dang,Dongxian Guan,Yuqin Men,Shuwen Jiang,Cong Jiang,Xiaoming Dai,Jing Liu,Zhen Wang,Peiqiang Yan,Jingchao Wang,Zhenbo Tu,Mrigya Babuta,Emily C. Erickson,Alissandra L. Hillis,Christian C. Dibble,John M. Asara,Gyongy Szabo,Piotr Siciński,Ji Miao,Yu-Ru Lee,Lifeng Pan,Reuben J. Shaw,Junying Yuan,Wenyi Wei
摘要
Adenosine monophosphate-activated protein kinase (AMPK) activity is stimulated to promote metabolic adaptation upon energy stress. However, sustained metabolic stress may cause cell death. The mechanisms by which AMPK dictates cell death are not fully understood. We report that metabolic stress promoted receptor-interacting protein kinase 1 (RIPK1) activation mediated by TRAIL receptors, whereas AMPK inhibited RIPK1 by phosphorylation at Ser