α-Synuclein-dependent increases in PIP5K1γ drive inositol signaling to promote neurotoxicity.

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作者： Jonathan D,Horvath ^[1] ; Maria,Casas ^[1] ; Candice,Kutchukian ^[1] ; Sara Creus,Sánchez ^[1] ; Melissa R,Pergande ^[2] ; Stephanie M,Cologna ^[2] ; Sergi,Simó ^[3] ; Rose E,Dixon ^[1] ; Eamonn J,Dickson ^[4]

作者单位： Department of Physiology and Membrane Biology, University of California, Davis, Davis, CA 95616, USA. ^[1] Department of Chemistry, University of Illinois, Chicago, IL, USA. ^[2] Department of Cell Biology and Human Anatomy, University of California, Davis, Davis, CA 95616, USA. ^[3] Department of Physiology and Membrane Biology, University of California, Davis, Davis, CA 95616, USA. Electronic address: ejdickson@ucdavis.edu. ^[4]

关键词 CP: Neuroscience IP(3)PIP5K calcium membrane contact sites neurodegeneration phosphoinositide PI(4,5)P(2)α-Syn

主题词人类(Humans);α突触核蛋白(alpha-Synuclein);神经元(Neurons);帕金森病(Parkinson Disease);磷脂酰肌醇4,5-二磷酸(Phosphatidylinositol 4,5-Diphosphate);信号传导(Signal Transduction);磷酸转移酶类(醇族体)(Phosphotransferases (Alcohol Group Acceptor))

DOI 10.1016/j.celrep.2023.113244

PMID 37838947

发布时间 2024-04-25

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