L
Liming Sun
Researcher at Chinese Academy of Sciences
Publications - 20
Citations - 4137
Liming Sun is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Necroptosis & Signal transduction. The author has an hindex of 10, co-authored 15 publications receiving 3232 citations.
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Journal ArticleDOI
Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase
Liming Sun,Huayi Wang,Zhigao Wang,Sudan He,She Chen,Daohong Liao,Lai Wang,Jiacong Yan,Weilong Liu,Xiaoguang Lei,Xiaodong Wang +10 more
TL;DR: The identification of a small molecule called necrosulfonamide that specifically blocks necrosis downstream of RIP3 activation is reported, which implicate MLKL as a key mediator of necrosis signaling downstream of the kinase RIP3.
Journal ArticleDOI
Mixed Lineage Kinase Domain-like Protein MLKL Causes Necrotic Membrane Disruption upon Phosphorylation by RIP3
TL;DR: The development of a monoclonal antibody that specifically recognizes phosphorylated MLKL in cells dying of this pathway and in human liver biopsy samples from patients suffering from drug-induced liver injury is reported.
Journal ArticleDOI
Pathogen blocks host death receptor signalling by arginine GlcNAcylation of death domains
Shan Li,Li Zhang,Qing Yao,Lin Li,Na Dong,Jie Rong,Wenqing Gao,Xiaojun Ding,Liming Sun,Xing Chen,She Chen,Feng Shao +11 more
TL;DR: The mechanism of action of NleB represents a new model by which bacteria counteract host defences, and also a previously unappreciated post-translational modification.
Journal ArticleDOI
A plug release mechanism for membrane permeation by MLKL.
TL;DR: The results suggest that the four-helix bundle mediates membrane breakdown during necroptosis and that the sixth helix acts as a plug that prevents opening of the bundle and is released upon RIP3 phosphorylation.
Journal ArticleDOI
Necrosome core machinery: MLKL.
TL;DR: The key role of MLKL in necroptosis signaling sheds light on the logic underlying this unique “membrane-explosive” cell death pathway.