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Calmodulin limits pathogenic Na(+) channel persistent current
Increased “persistent” current, caused by delayed inactivation, through voltage-gated Na(+) (Na(V)) channels leads to cardiac arrhythmias or epilepsy. The underlying molecular contributors to these inactivation defects are poorly understood. Here, we show that calmodulin (CaM) binding to multiple si...
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| Опубликовано в: : | J Gen Physiol |
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| Главные авторы: | , , , |
| Формат: | Artigo |
| Язык: | Inglês |
| Опубликовано: |
The Rockefeller University Press
2017
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| Предметы: | |
| Online-ссылка: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5299624/ https://ncbi.nlm.nih.gov/pubmed/28087622 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1085/jgp.201611721 |
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