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本文引用的文献

1
Ca2+/calcineurin regulation of cloned vascular K ATP channels: crosstalk with the protein kinase A pathway.克隆的血管ATP敏感性钾通道的Ca2+/钙调磷酸酶调节：与蛋白激酶A途径的相互作用
Br J Pharmacol. 2009 Jun;157(4):554-64. doi: 10.1111/j.1476-5381.2009.00221.x. Epub 2009 May 7.
2
cAMP-dependent protein kinase phosphorylation produces interdomain movement in SUR2B leading to activation of the vascular KATP channel.环磷酸腺苷（cAMP）依赖性蛋白激酶磷酸化作用使磺脲类受体2B（SUR2B）发生结构域间移动，从而激活血管ATP敏感性钾通道（KATP通道）。
J Biol Chem. 2008 Mar 21;283(12):7523-30. doi: 10.1074/jbc.M709941200. Epub 2008 Jan 15.
3
PKA phosphorylation of SUR2B subunit underscores vascular KATP channel activation by beta-adrenergic receptors.SUR2B亚基的蛋白激酶A磷酸化突出了β-肾上腺素能受体对血管ATP敏感性钾通道的激活作用。
Am J Physiol Regul Integr Comp Physiol. 2007 Sep;293(3):R1205-14. doi: 10.1152/ajpregu.00337.2007. Epub 2007 Jun 27.
4
Transgenic expression of a dominant negative K(ATP) channel subunit in the mouse endothelium: effects on coronary flow and endothelin-1 secretion.在小鼠内皮细胞中显性负性K(ATP)通道亚基的转基因表达：对冠状动脉血流和内皮素-1分泌的影响。
FASEB J. 2007 Jul;21(9):2162-72. doi: 10.1096/fj.06-7821com. Epub 2007 Mar 6.
5
Reversal of life-threatening, drug-related potassium-channel syndrome by glibenclamide.
Lancet. 2005;365(9474):1873-5. doi: 10.1016/S0140-6736(05)66619-6.
6
Loss of endothelial KATP channel-dependent, NO-mediated dilation of endocardial resistance coronary arteries in pigs with left ventricular hypertrophy.左心室肥厚猪的心内膜阻力冠状动脉中，内皮细胞ATP敏感性钾通道依赖性、一氧化氮介导的舒张功能丧失。
Br J Pharmacol. 2004 Sep;143(2):285-91. doi: 10.1038/sj.bjp.0705937. Epub 2004 Aug 23.
7
Multisite phosphorylation mechanism for protein kinase A activation of the smooth muscle ATP-sensitive K+ channel.蛋白激酶A激活平滑肌ATP敏感性钾通道的多位点磷酸化机制。
Circ Res. 2004 May 28;94(10):1359-66. doi: 10.1161/01.RES.0000128513.34817.c4. Epub 2004 Apr 15.
8
Episodic coronary artery vasospasm and hypertension develop in the absence of Sur2 K(ATP) channels.在缺乏Sur2 K(ATP)通道的情况下，会出现发作性冠状动脉血管痉挛和高血压。
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Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1.通过破坏内向整流钾离子通道蛋白6.1构建变异型心绞痛小鼠模型。
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Calcium modulation of vascular smooth muscle ATP-sensitive K(+) channels: role of protein phosphatase-2B.血管平滑肌ATP敏感性钾通道的钙调节：蛋白磷酸酶2B的作用
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血管ATP敏感性钾通道：去磷酸化与失活

Vascular K ATP channels: dephosphorylation and deactivation.

作者信息

Tammaro Paolo

机构信息

Faculty of Life Sciences, University of Manchester, Manchester, UK.

出版信息

Br J Pharmacol. 2009 Jun;157(4):551-3. doi: 10.1111/j.1476-5381.2009.00204.x.

DOI:10.1111/j.1476-5381.2009.00204.x
PMID:19630834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2707967/
Abstract

Vascular ATP-sensitive potassium (K(ATP)) channels (Kir6.1/SUR2B) are regulated by both cell metabolism and chemical transmitters. They are the target for a number of vasodilators and vasoconstrictors whose mechanisms of action involve activation of protein kinase A (PKA) and protein kinase C (PKC), respectively. The article by Orie et al. in this issue of the BJP sheds new light on the (opposing) role of protein phosphatases in the regulation of this ion channel activity. Their data suggest that calcineurin, a Ca(2+)-dependent protein phosphatase, modulates Kir6.1/SUR2B by inhibiting PKA-dependent phosphorylation of the channel. This novel mechanism may provide a modulation opposing the action of vasodilators on the K(ATP) channel.

摘要

血管ATP敏感性钾（K(ATP)）通道（Kir6.1/SUR2B）受细胞代谢和化学递质的双重调节。它们是多种血管舒张剂和血管收缩剂的作用靶点，这些药物的作用机制分别涉及蛋白激酶A（PKA）和蛋白激酶C（PKC）的激活。Orie等人在本期《英国药理学杂志》上发表的文章为蛋白磷酸酶在调节该离子通道活性中的（相反）作用提供了新的线索。他们的数据表明，钙调神经磷酸酶，一种Ca(2+)依赖性蛋白磷酸酶，通过抑制通道的PKA依赖性磷酸化来调节Kir6.1/SUR2B。这种新机制可能提供一种与血管舒张剂对K(ATP)通道作用相反的调节作用。