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The quest to identify the mechanism underlying adrenergic regulation of cardiac Ca2+ channels.
Channels ( IF 3.3 ) Pub Date : 2020-03-21 , DOI: 10.1080/19336950.2020.1740502
Daniel Roybal 1, 2 , Jessica A Hennessey 1 , Steven O Marx 1, 2
Affiliation  

Activation of protein kinase A by cyclic AMP results in a multi-fold upregulation of CaV1.2 currents in the heart, as originally reported in the 1970's and 1980's. Despite considerable interest and much investment, the molecular mechanisms responsible for this signature modulation remained stubbornly elusive for over 40 years. A key manifestation of this lack of understanding is that while this regulation is readily apparent in heart cells, it has not been possible to reconstitute it in heterologous expression systems. In this review, we describe the efforts of many investigators over the past decades to identify the mechanisms responsible for the β-adrenergic mediated activation of voltage-gated Ca2+ channels in the heart and other tissues.

中文翻译:

探索肾上腺素能调节心脏 Ca2+ 通道的潜在机制。

正如 1970 年代和 1980 年代最初报道的那样,环状 AMP 激活蛋白激酶 A 会导致心脏中 CaV1.2 电流的多倍上调。尽管有相当大的兴趣和大量投资,但 40 多年来,负责这种特征调制的分子机制仍然顽固地难以捉摸。这种缺乏理解的一个关键表现是,虽然这种调节在心脏细胞中很明显,但不可能在异源表达系统中重建它。在这篇综述中,我们描述了过去几十年许多研究人员为确定 β 肾上腺素能介导的心脏和其他组织中电压门控 Ca2+ 通道激活的机制所做的努力。
更新日期:2020-04-20
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