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Mutation of colocalized residues of the pore helix and transmembrane segments S5 and S6 disrupt deactivation and modify inactivation of KCNQ1 K(+) channels
KCNQ1 (Kv 7.1) α-subunits and KCNE1 β-subunits co-assemble to form channels that conduct the slow delayed rectifier K(+) current (I(Ks)) in the heart. Mutations in either subunit cause long QT syndrome (LQTS), an inherited disorder of cardiac repolarization. Here, the functional consequences of the...
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| Main Authors: | , , , |
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| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
Blackwell Science Inc
2005
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1665586/ https://ncbi.nlm.nih.gov/pubmed/15649981 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1113/jphysiol.2004.080887 |
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