Modulation of Kv4.3 current by accessory subunits

被引：125

作者：

Deschênes, I ^{[1
]}

Tomaselli, GF ^{[1
]}

机构：

[1] Johns Hopkins Univ, Dept Med, Inst Mol Cardiobiol, Div Cardiol, Baltimore, MD 21205 USA

来源：

FEBS LETTERS | 2002年 / 528卷 / 1-3期

关键词：

ion channel; potassium; accessory subunit;

D O I：

10.1016/S0014-5793(02)03296-9

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：

Kv4.3 encodes the pore-forming subunit of the cardiac transient outward potassium current (I-t0). hKv4.3-encoded current does not fully replicate cardiac It, suggesting a functionally significant role for accessory subunits. KChIP2 associates with Kv4.3 and modifies hKv4.3-encoded currents but does not replicate native I-t0. We examined the effect of several ancillary subunits expressed in the heart on hKv4.3-encoded currents. Remarkably, the ancillary subunits Kvbeta(3), minK, MiRP-1, the Na channel beta(1) and KChIP2 increased the density and modified the gating of hKv4.3 current. hKv4.3 promiscuously assembles with ancillary subunits in vitro, functionally modifying the encoded currents; however, the physiological significance is uncertain. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：183 / 188

页数：6

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