Article
Calmodulin activation limits the rate of KCNQ2 K+ channel exit from the endoplasmic reticulum.
The Journal of biological chemistry - 31 Jul 2009
Alaimo Alessandro, Gómez-Posada Juan Camilo, Aivar Paloma, Etxeberría Ainhoa, Rodriguez-Alfaro Jose Angel, Areso Pilar, Villarroel Alvaro
Abstract excerpt
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 human benign neonatal convulsions, perturbs CaM binding to KCNQ2 channels and prevents their correct trafficking to...
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