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An Epilepsy-Associated KCNT1 Mutation Enhances Excitability of Human iPSC-Derived Neurons by Increasing Slack K(Na) Currents
Mutations in the KCNT1 (Slack, K(Na)1.1) sodium-activated potassium channel produce severe epileptic encephalopathies. Expression in heterologous systems has shown that the disease-causing mutations give rise to channels that have increased current amplitude. It is not known, however, whether such g...
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| 出版年: | J Neurosci |
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| 主要な著者: | , , , , , , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Society for Neuroscience
2019
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| 主題: | |
| オンライン・アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6759030/ https://ncbi.nlm.nih.gov/pubmed/31350261 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.1628-18.2019 |
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