Long QT mutations at the interface between KCNQ1 helix C and KCNE1 disrupt I(KS) regulation by PKA and PIP(2)

KCNQ1 and KCNE1 co-assembly generates the I(KS) K(+) current, which is crucial to the cardiac action potential repolarization. Mutations in their corresponding genes cause long QT syndrome (LQT) and atrial fibrillation. The A-kinase anchor protein, yotiao (also known as AKAP9), brings the I(KS) chan...

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Shranjeno v:
Bibliografske podrobnosti
izdano v:J Cell Sci
Main Authors: Dvir, Meidan, Strulovich, Roi, Sachyani, Dana, Ben-Tal Cohen, Inbal, Haitin, Yoni, Dessauer, Carmen, Pongs, Olaf, Kass, Robert, Hirsch, Joel A., Attali, Bernard
Format: Artigo
Jezik:Inglês
Izdano: The Company of Biologists 2014
Teme:
Research Article
Online dostop:https://ncbi.nlm.nih.gov/pmc/articles/PMC6519428/
https://ncbi.nlm.nih.gov/pubmed/25037568
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1242/jcs.147033
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