The Noonan syndrome-associated D61G variant of the protein tyrosine phosphatase SHP2 prevents synaptic down-scaling.

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作者： Wen,Lu ^[1] ; Heng,Ai ^[2] ; Fusheng,Xue ^[3] ; Yifei,Luan ^[4] ; Bin,Zhang ^[3]

作者单位： Department of Biochemistry and Molecular Biology, Hainan Medical University, Haikou, China. ^[1] Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, China. ^[2] Department of Physiology, Hangzhou Medical College, Hangzhou, Zhejiang, China. ^[3] Zhejiang Key Laboratory of Organ Development and Regeneration, Institute of Life Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, China. ^[4] Zhejiang Key Laboratory of Organ Development and Regeneration, Institute of Life Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, China zhangbin890124@163.com. ^[5]

关键词 SHP2 Src homology 2 domain (SH2 domain)phosphatase phosphorylation phosphotyrosine signaling postsynaptic density protein 95 (PSD95)protein tyrosine phosphatase non-receptor type 11 (PTPN11)synaptic scaling α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA receptor)

主题词氨基酸取代(Amino Acid Substitution);动物(Animals);小鼠(Mice);突变, 误义(Mutation, Missense);努南综合征(Noonan Syndrome);蛋白质酪氨酸磷酸酶, 非受体11型(Protein Tyrosine Phosphatase, Non-Receptor Type 11);突触(Synapses)

DOI 10.1074/jbc.RA119.010331

PMID 32499374

发布时间 2021-07-18

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