Working model for the structural basis for KCNE1 modulation of the KCNQ1 potassium channel

被引：30

作者：

Van Horn, Wade D. ^{[1
]}

Vanoye, Carlos G. ^{[2
]}

Sanders, Charles R. ^{[1
]}

机构：

[1] Vanderbilt Univ, Dept Biochem, Sch Med, Nashville, TN 37232 USA

[2] Vanderbilt Univ, Dept Med, Sch Med, Nashville, TN 37232 USA

来源：

CURRENT OPINION IN STRUCTURAL BIOLOGY | 2011年 / 21卷 / 02期

关键词：

LONG-QT SYNDROME; I-KS CHANNELS; ATRIAL-FIBRILLATION; VOLTAGE SENSOR; K+ CHANNEL; FUNCTIONAL-CHARACTERIZATION; PROTEIN-INTERACTION; CARDIAC-ARRHYTHMIA; PERIODIC PARALYSIS; CRYSTAL-STRUCTURE;

D O I：

10.1016/j.sbi.2011.01.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The voltage-gated potassium channel KCNQ1 (Kv7.1) is modulated by KCNE1 (minK) to generate the I-Ks current crucial to heartbeat. Defects in either protein result in serious cardiac arrhythmias. Recently developed structural models of the open and closed state KCNQ1/KCNE1 complexes offer a compelling explanation for how KCNE1 slows channel opening and provides a platform from which to refine and test hypotheses for other aspects of KCNE1 modulation. These working models were developed using an integrative approach based on results from nuclear magnetic resonance spectroscopy, electrophysiology, biochemistry, and computational methods-an approach that can be applied iteratively for model testing and revision. We present a critical review of these structural models, illustrating the strengths and challenges of the integrative approach.

引用

页码：283 / 291

页数：9

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