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5篇 您的检索式:作者名="Liming She"
    题名 作者 年代 出处 被引量
1Myofiber necroptosis promotes muscle stem cell proliferation via releasing Tenascin-C during regeneration显示文摘Necroptosis,a form of programmed cell death,is characterized by the loss of membrane integrity and release of intracellular contents,the execution of which depends on the membrane-disrupting activity of the Mixed Lineage Kinase Domain-Like protein(MLKL)upon its phosphorylation.Here we found myofibers committed MLKL-dependent necroptosis after muscle injury.Either pharmacological inhibition of the necroptosis upstream kinase Receptor Interacting Protein Kinases 1(RIPK1)or genetic ablation of MLKL expression in myofibers led to significant muscle regeneration defects.By releasing factors into the muscle stem cell(MuSC)microenvironment,necroptotic myofibers facilitated muscle regeneration.Tenascin-C(TNC),released by necroptotic myofibers,was found to be critical for MuSC proliferation.The temporary expression of TNC in myofibers is tightly controlled by necroptosis;the extracellular release of TNC depends on necroptotic membrane rupture.TNC directly activated EGF receptor(EGFR)signaling pathway in MuSCs through its N-terminus assembly domain together with the EGF-like domain.These findings indicate that necroptosis plays a key role in promoting MuSC proliferation to facilitate muscle regeneration.Shen'ao Zhou Wei Zhang Gaihong Cai Yingzhe Ding Caixia Wei Sheng Li Yu Yang Jie Qin Dan Liu Hao Zhang Xiexiang Shao Jianhua Wang Hongye Wang Wenjun Yang Huating Wang She Chen Ping Hu Liming Sun 2020Cell Research2020,30,12:4
2Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase显示文摘Liming Sun Huayi Wang Zhigao Wang Sudan He She Chen Daohong Liao Lai Wang Jiacong Yan Weilong Liu Xiaoguang Lei Xiaodong Wang 2012Cell2012,,1:2
3Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase显示文摘Liming Sun Huayi Wang Zhigao Wang Sudan He She Chen Daohong Liao Lai Wang Jiacong Yan Weilong Liu Xiaoguang Lei Xiaodong Wang 2012Cell2012,,1:1
4A Systematic Investigation of Complement and Coagulation-Related Protein in Autism Spectrum Disorder Using Multiple Reaction Monitoring Technology显示文摘Autism spectrum disorder(ASD)is one of the common neurodevelopmental disorders in children.Its etiology and pathogenesis are poorly understood.Previous studies have suggested potential changes in the complement and coagulation pathways in individuals with ASD.In this study,using multiple reactions monitoring proteomic technology,16 of the 33 proteins involved in this pathway were identified as differentially-expressed proteins in plasma between children with ASD and controls.Among them,CFHR3,C4BPB,C4BPA,CFH,C9,SERPIND1,C8A,F9,and F11 were found to be altered in the plasma of children with ASD for the first time.SERPIND1 expression was positively correlated with the CARS score.Using the machine learning method,we obtained a panel composed of 12 differentially-expressed proteins with diagnostic potential for ASD.We also reviewed the proteins changed in this pathway in the brain and blood of patients with ASD.The complement and coagulation pathways may be activated in the peripheral blood of children with ASD and play a key role in the pathogenesis of ASD.Xueshan Cao Xiaoxiao Tang Chengyun Feng Jing Lin Huajie Zhang Qiong Liu Qihong Zheng Hongbin Zhuang Xukun Liu Haiying Li Naseer Ullah Khan Liming She 2023Neuroscience Bulletin2023,39,11:1
5Spontaneous necroptosis and autoinflammation are blocked by an inhibitory phosphorylation on MLKL during neonatal development显示文摘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.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 2022Cell Research2022,32,4:1
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