Spontaneous necroptosis and autoinflammation are blocked by an inhibitory phosphorylation on MLKL during neonatal development  

作　　者：Xinxin Zhu Na Yang Yu Yang Feiyang Yuan Dandan Yu Yu Zhang Zhaoqian Shu Ning Nan Hong Hu Xiaoyan Liu She Chen Liming Sun Huayi Wang 

机构地区：[1]School of Life Science and Technology,ShanghaiTech University,Shanghai,China [2]State Key Laboratory of Cell Biology,CAS Center for Excellence in Molecular Cell Science,Shanghai Institute of Biochemistry and Cell Biology,Chinese Academy of Sciences,University of Chinese Academy of Sciences,Shanghai,China [3]University of Chinese Academy of Sciences,Beijing,China [4]National Institute of Biological Sciences,Beijing,China [5]Tsinghua Institute of Multidisciplinary Biomedical Research,Tsinghua University,Beijing,China

出　　处：《Cell Research》2022年第4期407-410,共4页细胞研究（英文版）

基　　金：supported by the National Natural Science Foundation of China(32050187 to L.S.,31571427 to H.W.);the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA16020402 and XDB19020112 to L.S.)。

摘　　要：Dear Editor,Necroptosis,a form of caspase-independent cell death,is tightly regulated to maintain tissue homeostasis.The execution of necroptosis depends on receptor interacting protein kinase 3(RIP3)-activated mixed lineage kinase domain-like protein(MLKL).MLKL is phosphorylated by RIP3,which releases MLKL autoinhibi-tion and drives its self-oligomerization.1-3 Oligomerized MLKL translocates to cellular membranes,where it disrupts membrane integrity causing necroptotic cell death.

关 键 词：MLKL inflammation HOMEOSTASIS 

分 类 号：R36[医药卫生—病理学]