MaxiK channel and cell signalling.
MaxiK channel and cell signalling.
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DOI：
10.1007/s00424-013-1359-0
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发表时间：
2014-05
影响因子：
4.5
通讯作者：
Stefani, Enrico
中科院分区：
文献类型：
--
作者：
Toro, Ligia;Li, Min;Zhang, Zhu;Singh, Harpreet;Wu, Yong;Stefani, Enrico
关键词：
当我们了解大电导 Ca2+- 和电压激活 K+（MaxiK、BK、BKCa、Slo1、KCa1.1）通道如何与质膜上以及包括内质网、细胞核和线粒体在内的细胞内细胞器中的多种蛋白质相互作用时，该通道在细胞信号传导中的作用变得越来越明显。在这篇综述中，我们重点关注 MaxiK 通道与七个跨膜 G 蛋白偶联受体的相互作用，并讨论了表明通道大 C 端可能充当信号分子核的信息，包括与细胞死亡和存活相关的激酶。越来越多的证据表明，该通道能够与多种受体结合，包括β-肾上腺素受体、G蛋白偶联雌激素受体、乙酰胆碱受体、血栓素A2受体和血管紧张素II受体，这突显了该通道具有（或可能具有）的多种功能，不仅调节肌肉细胞的收缩/松弛或大脑中的神经传递，而且还调节细胞代谢、增殖、迁移和基因表达。与这一观点一致的是，MaxiK 通道与肥胖以及脑癌、前列腺癌和乳腺癌有关。更好地了解 MaxiK 通道异常（例如某些癌症中的过度表达）潜在或触发的分子机制可能会带来预防毁灭性疾病的新疗法。
The large-conductance Ca2+- and voltage-activated K+ (MaxiK, BK, BKCa, Slo1, KCa1.1) channel role in cell signalling is becoming apparent as we learn how the channel interacts with a multiplicity of proteins not only at the plasma membrane but in intracellular organelles including the endoplasmic reticulum, nucleus and mitochondria. In this review, we focus on the interactions of MaxiK channels with seven transmembrane G-protein coupled receptors, and discuss information suggesting that the channel big C-terminus may act as nucleus of signalling molecules including kinases relevant for cell death and survival. Increasing evidence indicates that the channel is able to associate with a variety of receptors including β-adrenergic receptors, G-protein coupled estrogen receptors, acetylcholine receptors, thromboxane A2 receptors and angiotensin II receptors, which highlights the varied functions that the channel has (or may have) not only in regulating contraction/relaxation of muscle cells or neurotransmission in the brain but also in cell metabolism, proliferation, migration and gene expression. In line with this view, MaxiK channels have been implicated in obesity and in brain, prostate, and mammary cancers. A better understanding of the molecular mechanisms underlying or triggered by MaxiK channel abnormalities like overexpression in certain cancers may lead to new therapeutics to prevent devastating diseases.
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影响因子：
2.5
作者：
Cibulsky, SA;Fei, H;Levitan, IB
通讯作者：
Levitan, IB
影响因子：
8.3
作者：
Francois, H;Athirakul, K;Coffman, TM
通讯作者：
Coffman, TM
影响因子：
8
作者：
Bloch, M.;Ousingsawat, J.;Bubendorf, L.
通讯作者：
Bubendorf, L.
影响因子：
4.4
作者：
Ge, Lisheng;Hoa, Neil T.;Jadus, Martin R.
通讯作者：
Jadus, Martin R.
DOI：
10.1073/pnas.89.22.11051
发表时间：
1992-11-15
影响因子：
11.1
作者：
KUME, H;GRAZIANO, MP;KOTLIKOFF, MI
通讯作者：
KOTLIKOFF, MI