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The modulation of the rate of inactivation of the mKv1.1 K+ channel by the β subunit, Kvβ1 and lack of effect of a Kvβ1 N‐terminal peptide

机译:β亚基Kvβ1对mKv1.1 K +通道失活速率的调节和缺乏Kvβ1N末端肽的作用

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>The coexpression of the rat Kvβ1 subunit with the mouse Kv1.1 (mKv1.1) K+ channel in Chinese hamster ovary cells caused an increase in the rate of inactivation of whole-cell current. Current decayed in a bi-exponential fashion with a fast voltage-dependent and a slower voltage-independent component. The inactivating current component accounted for around 40% of the total outward current. In contrast to previous studies using K+ channel α subunits, peptides based on the N-terminal of the Kvβ1 subunit were unable to mimic the action of the entire subunit. The findings indicate differences between the inactivation induced by the Kvβ1 subunit and the N-type inactivation mechanism associated with certain rapidly-inactivating cloned K+ channel α subunits.
机译:>大鼠仓鼠卵巢细胞中大鼠Kvβ1亚基与小鼠Kv1.1(mKv1.1)K + 通道的共表达导致全细胞电流失活率增加。电流以双指数方式衰减,具有快速的电压相关和较慢的电压独立成分。灭活电流分量约占总向外电流的40%。与以前使用K + 通道α亚基的研究相比,基于Kvβ1亚基N末端的肽无法模拟整个亚基的作用。这些发现表明,Kvβ1亚基诱导的失活与某些快速失活的克隆的K + 通道α亚基相关的N型失活机制之间存在差异。

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