Volume 32, No 4, Apr 2022

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 32 Issue 4, April 2022: 407-410   |  Open Access

LETTERS TO THE EDITOR

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

Xinxin Zhu^1,2,3 , Na Yang^2,3 , Yu Yang^2,3 , Feiyang Yuan^1,2,3 , Dandan Yu^1,3 , Yu Zhang^1,2,3 , Zhaoqian Shu^1,3 , Ning Nan^1,2,3 , Hong Hu¹ , Xiaoyan Liu¹ , She Chen^4,5 , Liming Sun^2,3,* , Huayi Wang^1,*

¹School of Life Science and Technology, ShanghaiTech University, Shanghai, China
²State 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
³University of Chinese Academy of Sciences, Beijing, China
⁴National Institute of Biological Sciences, Beijing, China
⁵Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, Beijing, China
Correspondence: Liming Sun(liming.sun@sibcb.ac.cn)Huayi Wang(wanghuayi@shanghaitech.edu.cn)

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 autoinhibition and drives its self-oligomerization.1,2,3 Oligomerized MLKL translocates to cellular membranes, where it disrupts membrane integrity causing necroptotic cell death.2,3

https://doi.org/10.1038/s41422-021-00583-w

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