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DCC-Mediated Dab1 Phosphorylation Participates in the Multipolar-to-Bipolar Transition of Migrating Neurons.
Zhang, Jian-Hua; Zhao, Yi-Fei; He, Xiao-Xiao; Zhao, Yang; He, Zi-Xuan; Zhang, Lei; Huang, Ying; Wang, Yu-Bing; Hu, Ling; Liu, Lin; Yu, Hua-Li; Xu, Jia-Hui; Lai, Ming-Ming; Zhao, Dong-Dong; Cui, Lei; Guo, Wei-Xiang; Xiong, Wen-Cheng; Ding, Yu-Qiang; Zhu, Xiao-Juan.
Afiliación
  • Zhang JH; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Zhao YF; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • He XX; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Zhao Y; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • He ZX; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Zhang L; Key Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.
  • Huang Y; Key Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.
  • Wang YB; Key Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.
  • Hu L; Key Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China.
  • Liu L; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Yu HL; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Xu JH; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Lai MM; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Zhao DD; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Cui L; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China.
  • Guo WX; State Key Laboratory for Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
  • Xiong WC; Department of Neurology, Georgia Regents University, Augusta, GA, USA; Department of Neuroscience, School of Medicine, Case Western Reserve University, Cleveland, OH 44120, USA.
  • Ding YQ; Key Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine, Shanghai 200092, China; Institute of Brain Sciences, Fudan University, Shanghai 200031, China. Ele
  • Zhu XJ; Key Laboratory of Molecular Epigenetics, Ministry of Education, Institute of Genetics and Cytology, Northeast Normal University, Changchun 130021, China. Electronic address: zhuxj720@nenu.edu.cn.
Cell Rep ; 22(13): 3598-3611, 2018 03 27.
Article en En | MEDLINE | ID: mdl-29590626
ABSTRACT
Newborn neurons undergo inside-out migration to their final destinations during neocortical development. Reelin-induced tyrosine phosphorylation of disabled 1 (Dab1) is a critical mechanism controlling cortical neuron migration. However, the roles of Reelin-independent phosphorylation of Dab1 remain unclear. Here, we report that deleted in colorectal carcinoma (DCC) interacts with Dab1 via its P3 domain. Netrin 1, a DCC ligand, induces Dab1 phosphorylation at Y220 and Y232. Interestingly, knockdown of DCC or truncation of its P3 domain dramatically delays neuronal migration and impairs the multipolar-to-bipolar transition of migrating neurons. Notably, the migration delay and morphological transition defects are rescued by the expression of a phospho-mimetic Dab1 or a constitutively active form of Fyn proto-oncogene (Fyn), a member of the Src-family tyrosine kinases that effectively induces Dab1 phosphorylation. Collectively, these findings illustrate a DCC-Dab1 interaction that ensures proper neuronal migration during neocortical development.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neocórtex / Receptor DCC / Proteínas del Tejido Nervioso / Neuronas Límite: Animals / Female / Humans Idioma: En Revista: Cell Rep Año: 2018 Tipo del documento: Article País de afiliación: China
Texto completo
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neocórtex / Receptor DCC / Proteínas del Tejido Nervioso / Neuronas Límite: Animals / Female / Humans Idioma: En Revista: Cell Rep Año: 2018 Tipo del documento: Article País de afiliación: China