Human Hyperekplexic Mutations in Glycine Receptors Disinhibit the Brainstem by Hijacking GABAA Receptors-Reference-Cited by-同舟云学术

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Human Hyperekplexic Mutations in Glycine Receptors Disinhibit the Brainstem by Hijacking GABAA Receptors

Published:2019-09 Issue: Volume:19 Page:634-646
ISSN:2589-0042
Container-title:iScience
language:en
Short-container-title:iScience

Author:

Zou Guichang,Chen Qi,Chen Kai,Zuo Xin,Ge Yushu,Hou Yiwen,Pan Tao,Pan Huilin,Liu Dan,Zhang Li,Xiong Wei

Funder

National Key R&D Program of China

National Natural Science Foundation of China

Chinese Academy of Sciences

Fundamental Research Funds for the Central Universities

Development Foundation of Hefei Center for Physical Science and Technology

Publisher

Elsevier BV

Subject

Multidisciplinary

Reference55 articles.

1. Transient neuromotor phenotype in transgenic spastic mice expressing low levels of glycine receptor β-subunit: an animal model of startle disease;Becker;Eur. J. Neurosci.,2000

2. Disease-specific human glycine receptor α1 subunit causes hyperekplexia phenotype and impaired glycine- and GABAA-receptor transmission in transgenic mice;Becker;J. Neurosci.,2002

3. How to build a glycinergic postsynaptic membrane;Betz;J. Cell Sci. Suppl.,1991

4. Inherited SHQ1 mutations impair interaction with NAP57/dyskerin, a major target in dyskeratosis congenita;Bizarro;Mol. Genet. Genomic Med.,2017

5. The impact of human hyperekplexia mutations on glycine receptor structure and function;Bode;Mol. Brain,2014

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3. Startle Disease: New Molecular Insights into an Old Neurological Disorder;The Neuroscientist;2022-06-25

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