Centre for Molecular Simulations, Department of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Centre for Molecular Simulations, Department of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Biochim Biophys Acta Proteins Proteom. 2017 Nov;1865(11 Pt B):1643-1653. doi: 10.1016/j.bbapap.2017.08.008. Epub 2017 Aug 26.
The rapid development of experimental and computational techniques has changed fundamentally our understanding of cellular-membrane transport. The advent of powerful computers and refined force-fields for proteins, ions, and lipids has expanded the applicability of Molecular Dynamics (MD) simulations. A myriad of cellular responses is modulated through the binding of endogenous and exogenous ligands (e.g. neurotransmitters and drugs, respectively) to ion channels. Deciphering the thermodynamics and kinetics of the ligand binding processes to these membrane proteins is at the heart of modern drug development. The ever-increasing computational power has already provided insightful data on the thermodynamics and kinetics of drug-target interactions, free energies of solvation, and partitioning into lipid bilayers for drugs. This review aims to provide a brief summary about modeling approaches to map out crucial binding pathways with intermediate conformations and free-energy surfaces for drug-ion channel binding mechanisms that are responsible for multiple effects on cellular functions. We will discuss post-processing analysis of simulation-generated data, which are then transformed to kinetic models to better understand the molecular underpinning of the experimental observables under the influence of drugs or mutations in ion channels. This review highlights crucial mathematical frameworks and perspectives on bridging different well-established computational techniques to connect the dynamics and timescales from all-atom MD and free energy simulations of ion channels to the physiology of action potentials in cellular models. This article is part of a Special Issue entitled: Biophysics in Canada, edited by Lewis Kay, John Baenziger, Albert Berghuis and Peter Tieleman.
实验和计算技术的快速发展从根本上改变了我们对细胞膜运输的理解。强大的计算机和改进的蛋白质、离子和脂质力场的出现扩展了分子动力学 (MD) 模拟的适用性。通过内源性和外源性配体(分别为神经递质和药物)与离子通道的结合,调节了无数的细胞反应。解析这些膜蛋白配体结合过程的热力学和动力学是现代药物开发的核心。不断增加的计算能力已经为药物靶标相互作用、溶剂化自由能以及药物进入脂质双层的分配的热力学和动力学提供了有见地的数据。本文旨在简要总结建模方法,以描绘与药物-离子通道结合机制相关的关键结合途径和自由能表面,该机制负责对细胞功能的多种影响。我们将讨论模拟生成数据的后处理分析,然后将其转换为动力学模型,以更好地了解在药物或离子通道突变的影响下实验观测值的分子基础。本文重点介绍了将不同成熟的计算技术联系起来的关键数学框架和观点,以连接从离子通道的全原子 MD 和自由能模拟到细胞模型中的动作电位生理学的动力学和时间尺度。本文是由 Lewis Kay、John Baenziger、Albert Berghuis 和 Peter Tieleman 编辑的特刊:加拿大生物物理学的一部分。