Loss of Katnal2 leads to ependymal ciliary hyperfunction and autism-related phenotypes in mice.

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作者： Ryeonghwa,Kang ^[1] ; Kyungdeok,Kim ^[2] ; Yewon,Jung ^[2] ; Sang-Han,Choi ^[1] ; Chanhee,Lee ^[3] ; Geun Ho,Im ^[4] ; Miram,Shin ^[3] ; Kwangmin,Ryu ^[3] ; Subin,Choi ^[5] ; Esther,Yang ^[1] ; Wangyong,Shin ^[5] ; Seungjoon,Lee ^[6] ; Suho,Lee ^[2] ; Zachary,Papadopoulos ^[2] ; Ji Hoon,Ahn ^[2] ; Gou Young,Koh ^[7] ; Jonathan,Kipnis ^[8] ; Hyojin,Kang ^[8] ; Hyun,Kim ^[7] ; Won-Ki,Cho ^[9] ; Soochul,Park ^[10] ; Seong-Gi,Kim ^[11] ; Eunjoon,Kim ^[6]

作者单位： Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea. ^[1] Center for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, Korea. ^[2] Center for Neuroscience Imaging Research, Institute for Basic Science (IBS), Suwon, Korea. ^[3] Department of Biomedical Engineering, Sungkyunkwan University, Suwon, Korea. ^[4] Department of Biological Sciences, Sookmyung Women's University, Seoul, Korea. ^[5] Department of Anatomy, Biomedical Sciences, College of Medicine, Korea University, Seoul, Korea. ^[6] Neuroscience Graduate Program, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America. ^[7] Center for Vascular Research, Institute for Basic Science (IBS), Daejeon, Korea. ^[8] Brain Immunology and Glia (BIG) Center, Washington University in St. Louis, St. Louis, Missouri, United States of America. ^[9] Department of Pathology and Immunology, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America. ^[10] Division of National Supercomputing, Korea Institute of Science and Technology Information (KISTI), Daejeon, Korea. ^[11]