L 型钙通道电流调控机制：扑朔迷离。
The L-type calcium channel current modulation mechanism: the plot thickens and fogs.
出版信息
J Clin Invest. 2019 Feb 1;129(2):496-498. doi: 10.1172/JCI125958. Epub 2019 Jan 7.
Abstract
Stressful situations provoke the fight-or-flight response, incurring rapid elevation of cardiac output via activation of protein kinase A (PKA). In this issue of the JCI, Yang et al. focus on the L-type calcium channel complex (LTCC), and their findings require reexamination of dogmatic principles. LTCC phosphorylation sites identified and studied to date are dispensable for PKA modulation of LTCC; however, a CaVβ2-CaV1.2 calcium channel interaction is now shown to be required. Yang et al. suggest a new hypothesis that LTCC modulation involves rearrangement of auxiliary proteins within the LTCC. However, we still do not know the targets of PKA that mediate LTCC modulation.
摘要
应激状态会引发战斗或逃跑反应，通过激活蛋白激酶 A（PKA）导致心输出量的快速升高。在本期 JCI 中，Yang 等人关注的是 L 型钙通道复合物（LTCC），他们的发现需要重新审视教条主义原则。迄今为止，已确定并研究的 LTCC 磷酸化位点对于 PKA 对 LTCC 的调节并非必不可少；然而，现在显示 CaVβ2-CaV1.2 钙通道相互作用是必需的。Yang 等人提出了一个新的假设，即 LTCC 的调节涉及 LTCC 内辅助蛋白的重排。然而，我们仍然不知道介导 LTCC 调节的 PKA 的靶标。
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