Laboratoire de Biologie et Modélisation de la Cellule, ENS de Lyon, Université Claude Bernard, CNRS UMR 5239, INSERM U1293, 46 Allée d'Italie Site Jacques Monod, F-69007 Lyon, France.
Research Group on Vestibular Pathophysiology, CNRS, Unit GDR2074, F-13331 Marseille, France.
Int J Mol Sci. 2024 Feb 14;25(4):2267. doi: 10.3390/ijms25042267.
Aquaporins (AQPs) constitute a wide family of water channels implicated in all kind of physiological processes. Zinc is the second most abundant trace element in the human body and a few studies have highlighted regulation of AQP0 and AQP4 by zinc. In the present work, we addressed the putative regulation of AQPs by zinc cations in silico through molecular dynamics simulations of human AQP0, AQP2, AQP4, and AQP5. Our results align with other scales of study and several in vitro techniques, hence strengthening the reliability of this regulation by zinc. We also described two distinct putative molecular mechanisms associated with the increase or decrease in AQPs' water permeability after zinc binding. In association with other studies, our work will help deciphering the interaction networks existing between zinc and channel proteins.
水通道蛋白（AQP）构成了一个广泛的家族，涉及各种生理过程。锌是人体内第二丰富的微量元素，有几项研究强调了锌对 AQP0 和 AQP4 的调节作用。在本工作中，我们通过对人 AQP0、AQP2、AQP4 和 AQP5 的分子动力学模拟，从计算的角度探讨了锌离子对 AQP 的可能调节作用。我们的结果与其他研究尺度和几种体外技术一致，因此加强了锌对其调节的可靠性。我们还描述了两种与锌结合后 AQP 水通透性增加或减少相关的独特的假定分子机制。结合其他研究，我们的工作将有助于破译锌与通道蛋白之间存在的相互作用网络。
