Two KCNQ2 Encephalopathy Variants in the Calmodulin-Binding Helix A Exhibit Dominant-Negative Effects and Altered PIP2 Interaction
Author:
Funder
National Institutes of Health
Publisher
Frontiers Media SA
Subject
Physiology (medical),Physiology
Reference78 articles.
1. A recurrent KCNQ2 pore mutation causing early onset epileptic encephalopathy has a moderate effect on M current but alters subcellular localization of Kv7 channels;Abidi;Neurobiol. Dis.,2015
2. Pivoting between calmodulin lobes triggered by calcium in the Kv7.2/calmodulin complex;Alaimo;PLoS One,2014
3. Calmodulin activation limits the rate of KCNQ2 K+ channel exit from the endoplasmic reticulum;Alaimo;J. Biol. Chem.,2009
4. Uncoupling PIP2-calmodulin regulation of Kv7.2 channels by an assembly destabilizing epileptogenic mutation;Alberdi;J. Cell Sci.,2015
5. Epilepsy-causing mutations in Kv7.2 C-terminus affect binding and functional modulation by calmodulin;Ambrosino;Biochim. Biophys. Acta,2015
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