Functional insights into modulation of BKCa channel activity to alter myometrial contractility.
Functional insights into modulation of BKCa channel activity to alter myometrial contractility.
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DOI：
10.3389/fphys.2014.00289
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发表时间：
2014
影响因子：
4
通讯作者：
England SK
中科院分区：
文献类型：
--
作者：
Lorca RA;Prabagaran M;England SK
大电导电压和Ca2+激活的K+通道（BKCa）是多种细胞和组织中膜兴奋性的重要调节剂。在子宫肌层平滑肌中，BKCa的激活在缓冲收缩力以维持妊娠期间的子宫静止以及在分娩开始时过渡到更具收缩力的状态中起着至关重要的作用。已经描述了多种调节机制以改变BKCa通道活性、表达和细胞定位。在子宫肌层中，BKCa受选择性剪接、靶向质膜的蛋白质、膜微区隔化和翻译后修饰的调节。此外，与辅助蛋白（即，β 1-和β 2-亚基）、与G蛋白偶联受体信号传导途径（如肾上腺素能和催产素受体激活的信号传导途径）的相关性以及激素调节提供了子宫肌层平滑肌中BKCa通道功能可变调节的进一步机制。在这里，我们提供了一个概述这些机制的BKCa通道调制，并提供了一个上下文，他们在子宫肌层功能。
The large-conductance voltage- and Ca2+-activated K+ channel (BKCa) is an important regulator of membrane excitability in a wide variety of cells and tissues. In myometrial smooth muscle, activation of BKCa plays essential roles in buffering contractility to maintain uterine quiescence during pregnancy and in the transition to a more contractile state at the onset of labor. Multiple mechanisms of modulation have been described to alter BKCa channel activity, expression, and cellular localization. In the myometrium, BKCa is regulated by alternative splicing, protein targeting to the plasma membrane, compartmentation in membrane microdomains, and posttranslational modifications. In addition, interaction with auxiliary proteins (i.e., β1- and β2-subunits), association with G-protein coupled receptor signaling pathways, such as those activated by adrenergic and oxytocin receptors, and hormonal regulation provide further mechanisms of variable modulation of BKCa channel function in myometrial smooth muscle. Here, we provide an overview of these mechanisms of BKCa channel modulation and provide a context for them in relation to myometrial function.
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影响因子：
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