Human Neuropsychiatric Disease Modeling using Conditional Deletion Reveals Synaptic Transmission Defects Caused by Heterozygous Mutations in NRXN1.

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作者： ChangHui,Pak ^[1] ; Tamas,Danko ^[2] ; Yingsha,Zhang ^[1] ; Jason,Aoto ^[1] ; Garret,Anderson ^[1] ; Stephan,Maxeiner ^[1] ; Fei,Yi ^[1] ; Marius,Wernig ^[3] ; Thomas C,Südhof ^[4]

作者单位： Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. ^[1] Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. ^[2] Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA; Department of Pathology, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. ^[3] Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA. Electronic address: tcs1@stanford.edu. ^[4]

关键词 autism human neurons iN cells neurexin schizophrenia synapse synaptic cell adhesion