CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression

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.

Bibliographic Details
Main Authors:	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
Format:	Article
Language:	English
Published:	Nature Publishing Group 2017-08-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/s41467-017-00368-z

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spelling	doaj-c1fec91be8b04fc981937dd1ca6abdea2021-05-11T07:07:32ZengNature Publishing GroupNature Communications2041-17232017-08-018111710.1038/s41467-017-00368-zCDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expressionYongqing Liu0Shirong Lai1Weining Ma2Wei Ke3Chan Zhang4Shumeng Liu5Yu Zhang6Fei Pei7Shaoyi Li8Ming Yi9Yousheng Shu10Yongfeng Shang11Jing Liang12Zhuo Huang13Key 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 CenterKey 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 CenterDepartment of Neurology, Shengjing Hospital Affiliated to China Medical UniversityState 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 UniversityNeuroscience Research Institute & Department of Neurobiology, Peking University Health Science CenterKey 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 CenterKey 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 CenterDepartment of Pathology, Peking University Health Science CenterDepartment of Neurology, Shengjing Hospital Affiliated to China Medical UniversityNeuroscience Research Institute & Department of Neurobiology, Peking University Health Science CenterState 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 UniversityKey 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 CenterKey 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 CenterKey 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 CenterAlterations 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.https://doi.org/10.1038/s41467-017-00368-z
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	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
spellingShingle	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 CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression Nature Communications
author_facet	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
author_sort	Yongqing Liu
title	CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
title_short	CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
title_full	CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
title_fullStr	CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
title_full_unstemmed	CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression
title_sort	cdyl suppresses epileptogenesis in mice through repression of axonal nav1.6 sodium channel expression
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2017-08-01
description	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.
url	https://doi.org/10.1038/s41467-017-00368-z
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CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression

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