Nature Communications (Aug 2017)
CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
- Yongqing Liu,
- Shirong Lai,
- Weining Ma,
- Wei Ke,
- Chan Zhang,
- Shumeng Liu,
- Yu Zhang,
- Fei Pei,
- Shaoyi Li,
- Ming Yi,
- Yousheng Shu,
- Yongfeng Shang,
- Jing Liang,
- Zhuo Huang
Affiliations
- Yongqing Liu
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Shirong Lai
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Weining Ma
- Department of Neurology, Shengjing Hospital Affiliated to China Medical University
- Wei Ke
- State Key Laboratory of Cognitive Neuroscience and Learning and IDG/McGovern Institute for Brain Research, School of Brain and Cognitive Sciences, the Collaborative Innovation Center for Brain Science, Beijing Normal University
- Chan Zhang
- Neuroscience Research Institute & Department of Neurobiology, Peking University Health Science Center
- Shumeng Liu
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Yu Zhang
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Fei Pei
- Department of Pathology, Peking University Health Science Center
- Shaoyi Li
- Department of Neurology, Shengjing Hospital Affiliated to China Medical University
- Ming Yi
- Neuroscience Research Institute & Department of Neurobiology, Peking University Health Science Center
- Yousheng Shu
- State Key Laboratory of Cognitive Neuroscience and Learning and IDG/McGovern Institute for Brain Research, School of Brain and Cognitive Sciences, the Collaborative Innovation Center for Brain Science, Beijing Normal University
- Yongfeng Shang
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Jing Liang
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- Zhuo Huang
- Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), State Key Laboratory of Natural and Biomimetic Drugs, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center
- DOI
- https://doi.org/10.1038/s41467-017-00368-z
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 17
Abstract
Alterations in intrinsic plasticity are important in epilepsy. Here the authors show that the epigenetic factor CDYL regulates the gene expression of the voltage gated sodium channel, Nav1.6, which contributes to seizures in a rat model of epilepsy.
