Disruption of Mbd5 in mice causes neuronal functional deficits and neurobehavioral abnormalities consistent with 2q23.1 microdeletion syndrome.

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作者： Vladimir,Camarena ^[1] ; Lei,Cao ^[1] ; Clemer,Abad ^[2] ; Alexander,Abrams ^[1] ; Yaima,Toledo ^[1] ; Kimi,Araki ^[3] ; Masatake,Araki ^[3] ; Katherina,Walz ^[4] ; Juan I,Young ^[5]

作者单位： Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miami, FL, USA. ^[1] John P. Hussman Institute for Human Genomics, Miller School of Medicine University of Miami, Miami, FL, USA. ^[2] Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan. ^[3] Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miami, FL, USA John P. Hussman Institute for Human Genomics, Miller School of Medicine University of Miami, Miami, FL, USA. ^[4] Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami, Miami, FL, USA John P. Hussman Institute for Human Genomics, Miller School of Medicine University of Miami, Miami, FL, USA jyoung3@med.miami.edu. ^[5]

关键词 MBD5 autistic disorder intellectual disability mouse model

主题词动物(Animals);染色体缺失(Chromosome Deletion);染色体, 哺乳动物(Chromosomes, Mammalian);基因缺失(Gene Deletion);甲基-CpG-结合蛋白质2(Methyl-CpG-Binding Protein 2);小鼠(Mice);神经系统疾病(Nervous System Diseases)

DOI 10.15252/emmm.201404044

PMID 25001218

发布时间 2021-10-21

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