Deschênes Isabelle, Tomaselli Gordon F
Department of Medicine, Institute of Molecular Cardiobiology, Division of Cardiology, Johns Hopkins University, Baltimore, MD 21205, USA.
FEBS Lett. 2002 Sep 25;528(1-3):183-8. doi: 10.1016/s0014-5793(02)03296-9.
Kv4.3 encodes the pore-forming subunit of the cardiac transient outward potassium current (I(to)). hKv4.3-encoded current does not fully replicate cardiac I(to), 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(to). 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.
Kv4.3编码心脏瞬时外向钾电流（I(to)）的孔形成亚基。hKv4.3编码的电流不能完全复制心脏I(to)，这表明辅助亚基具有功能上的重要作用。KChIP2与Kv4.3相关联并修饰hKv4.3编码的电流，但不能复制天然I(to)。我们研究了几种在心脏中表达的辅助亚基对hKv4.3编码电流的影响。值得注意的是，辅助亚基Kvbeta(3)、minK、MiRP-1、钠通道beta(1)和KChIP2增加了hKv4.3电流的密度并改变了其门控特性。hKv4.3在体外与辅助亚基随机组装，从功能上修饰编码的电流；然而，其生理意义尚不确定。
