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本文引用的文献

1
Cardiac L-type calcium channel (Cav1.2) associates with gamma subunits.心脏L型钙通道(Cav1.2)与γ亚基相关联。
FASEB J. 2011 Mar;25(3):928-36. doi: 10.1096/fj.10-172353. Epub 2010 Dec 2.
2
Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.钙内流通过 Cav1.2 是病理性心肌细胞肥大的近端信号。
J Mol Cell Cardiol. 2011 Mar;50(3):460-70. doi: 10.1016/j.yjmcc.2010.11.012. Epub 2010 Nov 25.
3
Multiple C-terminal tail Ca(2+)/CaMs regulate Ca(V)1.2 function but do not mediate channel dimerization.多个 C 末端尾部 Ca(2+)/CaMs 调节 Ca(V)1.2 功能,但不介导通道二聚化。
EMBO J. 2010 Dec 1;29(23):3924-38. doi: 10.1038/emboj.2010.260. Epub 2010 Oct 15.
4
Molecular mechanism of calcium channel regulation in the fight-or-flight response.战斗或逃跑反应中钙通道调节的分子机制。
Sci Signal. 2010 Sep 28;3(141):ra70. doi: 10.1126/scisignal.2001152.
5
Activation of NFATc1 is directly mediated by IP3 in adult cardiac myocytes.NFATc1 的激活是由 IP3 在成年心肌细胞中直接介导的。
Am J Physiol Heart Circ Physiol. 2010 Nov;299(5):H1701-7. doi: 10.1152/ajpheart.00470.2010. Epub 2010 Sep 17.
6
Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels.成人心肌细胞的交感刺激需要 AKAP5 与 L 型钙通道的亚群结合。
Circ Res. 2010 Sep 17;107(6):747-56. doi: 10.1161/CIRCRESAHA.109.216127. Epub 2010 Jul 29.
7
Quantitative proteomics of the Cav2 channel nano-environments in the mammalian brain.哺乳动物脑内 Cav2 通道纳米环境的定量蛋白质组学。
Proc Natl Acad Sci U S A. 2010 Aug 24;107(34):14950-7. doi: 10.1073/pnas.1005940107. Epub 2010 Jul 28.
8
Mitochondria control functional CaV1.2 expression in smooth muscle cells of cerebral arteries.线粒体控制脑动脉平滑肌细胞功能性 Cav1.2 表达。
Circ Res. 2010 Sep 3;107(5):631-41. doi: 10.1161/CIRCRESAHA.110.224345. Epub 2010 Jul 8.
9
Nifedipine inhibits cardiac hypertrophy and left ventricular dysfunction in response to pressure overload.硝苯地平抑制压力超负荷引起的心肌肥厚和左心室功能障碍。
J Cardiovasc Transl Res. 2010 Aug;3(4):304-13. doi: 10.1007/s12265-010-9182-x. Epub 2010 May 1.
10
Rem GTPase interacts with the proximal CaV1.2 C-terminus and modulates calcium-dependent channel inactivation.Rem GTPase 与近端 CaV1.2 C 末端相互作用,并调节钙依赖性通道失活。
Channels (Austin). 2010 May-Jun;4(3):192-202. doi: 10.4161/chan.4.3.11867. Epub 2010 May 1.

L 型钙通道转录的自动调节。

L-type calcium channel auto-regulation of transcription.

机构信息

Department of Physiology, MS-508, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536-0298, USA.

出版信息

Cell Calcium. 2011 May;49(5):306-13. doi: 10.1016/j.ceca.2011.01.001. Epub 2011 Feb 3.

DOI:10.1016/j.ceca.2011.01.001
PMID:21295347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3097264/
Abstract

L-type calcium channels (LTCC) impact the function of nearly all excitable cells. The classical LTCC function is to mediate trans-sarcolemmal Ca(2+) flux. This review focuses on the contribution of a mobile segment of the LTCC that regulates ion channel function, and also serves as a regulator of transcription in the nucleus. Specifically we highlight recent work demonstrating an auto-feedback regulatory pathway whereby the LTCC transcription factor regulates the LTCC. Also discussed is acute and long-term regulation of function by the LTCC-transcription regulator.

摘要

L 型钙通道 (LTCC) 影响几乎所有可兴奋细胞的功能。经典的 LTCC 功能是介导跨肌膜的 Ca(2+) 流动。本综述重点介绍了 LTCC 中一个可移动片段的贡献,该片段调节离子通道功能,同时也是核中转录的调节剂。具体来说,我们强调了最近的工作,证明了 LTCC 转录因子通过自动反馈调节途径调节 LTCC。还讨论了 LTCC-转录调节剂对功能的急性和长期调节。

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