使用基因工程小鼠进行兰尼碱受体研究。
Ryanodine receptor studies using genetically engineered mice.
机构信息
Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, New York, NY, USA.
出版信息
FEBS Lett. 2010 May 17;584(10):1956-65. doi: 10.1016/j.febslet.2010.03.005. Epub 2010 Mar 7.
Abstract
Ryanodine receptors (RyR) regulate intracellular Ca(2+) release in many cell types and have been implicated in a number of inherited human diseases. Over the past 15 years genetically engineered mouse models have been developed to elucidate the role that RyRs play in physiology and pathophysiology. To date these models have implicated RyRs in fundamental biological processes including excitation-contraction coupling and long term plasticity as well as diseases including malignant hyperthermia, cardiac arrhythmias, heart failure, and seizures. In this review we summarize the RyR mouse models and how they have enhanced our understanding of the RyR channels and their roles in cellular physiology and disease.
摘要
Ryanodine 受体 (RyR) 调节许多细胞类型中的细胞内 Ca(2+)释放，并与许多遗传性人类疾病有关。在过去的 15 年中，已经开发出了基因工程小鼠模型，以阐明 RyR 在生理学和病理生理学中的作用。迄今为止，这些模型已经表明 RyR 参与了包括兴奋-收缩偶联和长期可塑性在内的基本生物学过程，以及包括恶性高热、心律失常、心力衰竭和癫痫在内的疾病。在这篇综述中，我们总结了 RyR 小鼠模型，以及它们如何增强我们对 RyR 通道及其在细胞生理学和疾病中的作用的理解。
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Beta-adrenergic signaling accelerates and synchronizes cardiac ryanodine receptor response to a single L-type Ca2+ channel.β-肾上腺素能信号传导加速并同步心脏雷诺丁受体对单个L型Ca2+通道的反应。
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Membrane depolarization causes a direct activation of G protein-coupled receptors leading to local Ca2+ release in smooth muscle.膜去极化导致G蛋白偶联受体直接激活，进而引起平滑肌局部钙离子释放。
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