Reduced axonal surface expression and phosphoinositide sensitivity in K v 7 channels disrupts their function to inhibit neuronal excitability in Kcnq2 epileptic encephalopathy-Reference-Cited by-同舟云学术

Reduced axonal surface expression and phosphoinositide sensitivity in K v 7 channels disrupts their function to inhibit neuronal excitability in Kcnq2 epileptic encephalopathy

Published:2018-10 Issue: Volume:118 Page:76-93
ISSN:0969-9961
Container-title:Neurobiology of Disease
language:en
Short-container-title:Neurobiology of Disease

Author:

Kim Eung Chang,Zhang Jiaren,Pang Weilun,Wang Shuwei,Lee Kwan Young,Cavaretta John P.,Walters Jennifer,Procko Erik,Tsai Nien-Pei^ORCID,Chung Hee Jung^ORCID

Funder

National institute of Neurological Disorders and Stroke

Roy J. Carver Charitable Trust

Epilepsy Foundation

Publisher

Elsevier BV

Subject

Neurology

Reference115 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. Calmodulin activation limits the rate of KCNQ2 K+ channel exit from the endoplasmic reticulum;Alaimo;J. Biol. Chem.,2009

3. Alaimo, A., et al., 2012. Cooperativity between calmodulin binding sites in Kv7.2 channels. J. Cell Sci.