Suppr超能文献

在存在兰尼碱受体的情况下增强的二氢吡啶受体通道活性。

Enhanced dihydropyridine receptor channel activity in the presence of ryanodine receptor.

作者信息

Nakai J, Dirksen R T, Nguyen H T, Pessah I N, Beam K G, Allen P D

机构信息

Department of Medical Chemistry, Kyoto University Faculty of Medicine, Japan.

出版信息

Nature. 1996 Mar 7;380(6569):72-5. doi: 10.1038/380072a0.

Abstract

Excitation-contraction coupling in skeletal muscle involves a voltage sensor in the plasma membrane which, in response to depolarization, causes an intracellular calcium-release channel to open. The skeletal isoform of the ryanodine receptor (RyR-1) functions as the Ca2+-release channel and the dihydropyridine receptor (DHPR) functions as the voltage sensor and also as an L-type Ca2+ channel. Here we examine the possibility that there is a retrograde signal from RyR-1 to the DHPR, using myotubes from mice homozygous for a disrupted RyR-1 gene (dyspedic mice). As expected, we find that there is no excitation-contraction coupling in dyspedic myotubes, but we also find that they have a roughly 30-fold reduction in L-type Ca2+-current density. Injection of dyspedic myotubes with RyR-1 complementary DNA restores excitation-contraction coupling and causes the density of L-type Ca2+ current to rise towards normal. Despite the differences in Ca2+-current magnitude, measurements of charge movement indicate that the density of DHPRs is similar in dyspedic and RyR-1-expressing myotubes. Our results support the possibility of a retrograde signal by which RyR-1 enhances the function of DHPRs as Ca2+ channels.

摘要

骨骼肌中的兴奋-收缩偶联涉及质膜中的电压传感器,该传感器响应去极化,使细胞内钙释放通道打开。兰尼碱受体(RyR-1)的骨骼肌亚型作为Ca2+释放通道发挥作用,而二氢吡啶受体(DHPR)作为电压传感器以及L型Ca2+通道发挥作用。在这里,我们使用来自兰尼碱受体-1基因敲除纯合子小鼠(患肌营养不良症小鼠)的肌管,研究是否存在从RyR-1到DHPR的逆行信号。正如预期的那样,我们发现在患肌营养不良症的肌管中不存在兴奋-收缩偶联,但我们还发现它们的L型Ca2+电流密度大约降低了30倍。向患肌营养不良症的肌管中注射RyR-1互补DNA可恢复兴奋-收缩偶联,并使L型Ca2+电流密度恢复到正常水平。尽管Ca2+电流大小存在差异,但电荷移动测量表明,患肌营养不良症的肌管和表达RyR-1的肌管中DHPR的密度相似。我们的结果支持存在逆行信号的可能性,通过该信号RyR-1增强DHPR作为Ca2+通道的功能。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验