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Calmodulin Activation Limits the Rate of KCNQ2 K(+) Channel Exit from the Endoplasmic Reticulum
The potential regulation of protein trafficking by calmodulin (CaM) is a novel concept that remains to be substantiated. We proposed that KCNQ2 K(+) channel trafficking is regulated by CaM binding to the C-terminal A and B helices. Here we show that the L339R mutation in helix A, which is linked to...
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| Main Authors: | , , , , , , |
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| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
American Society for Biochemistry and Molecular Biology
2009
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2742831/ https://ncbi.nlm.nih.gov/pubmed/19494108 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1074/jbc.M109.019539 |
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