哺乳动物质子偶联肽转运体的作用机制。

The mechanism of mammalian proton-coupled peptide transporters.

机构信息

Structural Bioinformatics and Computational Biochemistry, Department of Biochemistry, University of Oxford, Oxford, United Kingdom.

The Kavli Institute for Nanoscience Discovery, University of Oxford, Oxford, United Kingdom.

出版信息

Elife. 2024 Jul 23;13:RP96507. doi: 10.7554/eLife.96507.

Abstract

Proton-coupled oligopeptide transporters (POTs) are of great pharmaceutical interest owing to their promiscuous substrate binding site that has been linked to improved oral bioavailability of several classes of drugs. Members of the POT family are conserved across all phylogenetic kingdoms and function by coupling peptide uptake to the proton electrochemical gradient. Cryo-EM structures and alphafold models have recently provided new insights into different conformational states of two mammalian POTs, SLC15A1, and SLC15A2. Nevertheless, these studies leave open important questions regarding the mechanism of proton and substrate coupling, while simultaneously providing a unique opportunity to investigate these processes using molecular dynamics (MD) simulations. Here, we employ extensive unbiased and enhanced-sampling MD to map out the full SLC15A2 conformational cycle and its thermodynamic driving forces. By computing conformational free energy landscapes in different protonation states and in the absence or presence of peptide substrate, we identify a likely sequence of intermediate protonation steps that drive inward-directed alternating access. These simulations identify key differences in the extracellular gate between mammalian and bacterial POTs, which we validate experimentally in cell-based transport assays. Our results from constant-PH MD and absolute binding free energy (ABFE) calculations also establish a mechanistic link between proton binding and peptide recognition, revealing key details underpining secondary active transport in POTs. This study provides a vital step forward in understanding proton-coupled peptide and drug transport in mammals and pave the way to integrate knowledge of solute carrier structural biology with enhanced drug design to target tissue and organ bioavailability.

摘要

质子偶联寡肽转运体(POTs)因其广泛的底物结合位点而引起了极大的药物研究兴趣,该结合位点与提高几类药物的口服生物利用度有关。POT 家族的成员在所有系统发育王国中都得到了保守,其通过将肽摄取与质子电化学梯度偶联来发挥作用。冷冻电镜结构和 alphafold 模型最近为两种哺乳动物 POTs(SLC15A1 和 SLC15A2)的不同构象状态提供了新的见解。然而,这些研究仍然存在关于质子和底物偶联机制的重要问题,同时为使用分子动力学(MD)模拟研究这些过程提供了独特的机会。在这里,我们采用广泛的无偏和增强采样 MD 来描绘 SLC15A2 完整构象循环及其热力学驱动力。通过在不同质子化状态下以及在不存在或存在肽底物的情况下计算构象自由能景观,我们确定了一个可能的中间质子化步骤序列,该序列驱动内向交替访问。这些模拟确定了哺乳动物和细菌 POTs 之间细胞外门之间的关键差异,我们通过基于细胞的转运测定实验对其进行了验证。我们来自恒 pH MD 和绝对结合自由能(ABFE)计算的结果还建立了质子结合与肽识别之间的机制联系,揭示了 POTs 中次级主动转运的关键细节。这项研究为理解哺乳动物中质子偶联肽和药物转运提供了重要的一步,并为整合溶质载体结构生物学知识与增强药物设计以靶向组织和器官生物利用度铺平了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e75/11265797/2cb9fa91d6cc/elife-96507-fig1.jpg

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