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本文引用的文献

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What keeps us ticking: a funny current, a calcium clock, or both?是什么驱动着我们:一种有趣的电流、一个钙时钟,还是两者皆有?
J Mol Cell Cardiol. 2009 Aug;47(2):157-70. doi: 10.1016/j.yjmcc.2009.03.022. Epub 2009 Apr 8.
2
A-kinase anchoring proteins: from protein complexes to physiology and disease.A激酶锚定蛋白:从蛋白质复合物到生理与疾病
IUBMB Life. 2009 Apr;61(4):394-406. doi: 10.1002/iub.168.
3
Mutation of an A-kinase-anchoring protein causes long-QT syndrome.一种A激酶锚定蛋白的突变会导致长QT综合征。
Proc Natl Acad Sci U S A. 2007 Dec 26;104(52):20990-5. doi: 10.1073/pnas.0710527105. Epub 2007 Dec 19.
4
Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel.KCNQ1-KCNE1钾通道β肾上腺素能受体调节所需的大分子信号复合物
Science. 2002 Jan 18;295(5554):496-9. doi: 10.1126/science.1066843.
5
Regulation of ion channels by cAMP-dependent protein kinase and A-kinase anchoring proteins.环磷酸腺苷(cAMP)依赖性蛋白激酶和A激酶锚定蛋白对离子通道的调控
Curr Opin Neurobiol. 1998 Jun;8(3):330-4. doi: 10.1016/s0959-4388(98)80057-3.

肾上腺素刺激在心脏中的分子机制。

Molecular mechanisms of adrenergic stimulation in the heart.

机构信息

Department of Pharmacology, Columbia University, New York, New York 10032, USA.

出版信息

Heart Rhythm. 2010 Aug;7(8):1151-3. doi: 10.1016/j.hrthm.2010.02.013. Epub 2010 Feb 13.

DOI:10.1016/j.hrthm.2010.02.013
PMID:20156590
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2891219/
Abstract

Increased cardiac output in response to beta-adrenergic receptor stimulation is achieved by rapid alteration of the activity of cardiac ion channels, pumps, and exchangers. Over the past decade, the discovery of macromolecular complexes, which include the ion channels and pumps and the kinases that control their level of phosphorylation, has led to an increased understanding of the molecular mechanisms behind the cardiac adrenergic response. The increased understanding has led to the discovery of a new long QT gene encoding an accessory protein in one of these macromolecular complexes. This article briefly reviews the major components of the beta-adrenergic pathway in the heart and discusses the direction of current and future research.

摘要

心脏对β肾上腺素能受体刺激的输出量增加是通过快速改变心脏离子通道、泵和交换器的活性来实现的。在过去的十年中,发现了包括离子通道和泵以及控制其磷酸化水平的激酶在内的大分子复合物,这使得人们对心脏肾上腺素能反应背后的分子机制有了更多的了解。这种深入的了解导致发现了一个新的长 QT 基因,该基因编码这些大分子复合物中的一个辅助蛋白。本文简要回顾了心脏中β肾上腺素能途径的主要组成部分,并讨论了当前和未来研究的方向。