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铁死亡抑制蛋白1活性通过其N-肉豆蔻酰化尾部的变构自调节。

Allosteric Autoregulation of Ferroptosis Suppressor Protein 1 Activity by its N-myristoylated Tail.

作者信息

Ventura Carlos, Bogetti Xiaowei, Lee Ji Young, Bahar Ivet

机构信息

Laufer Center for Physical and Quantitative Biology, Stony Brook University, Stony Brook, NY 11794, USA; Department of Chemistry, College of Arts & Sciences, Stony Brook University, Stony Brook, NY 11794, USA.

Laufer Center for Physical and Quantitative Biology, Stony Brook University, Stony Brook, NY 11794, USA.

出版信息

J Mol Biol. 2025 Jul 11:169344. doi: 10.1016/j.jmb.2025.169344.

Abstract

Ferroptosis is a form of cell death characterized by iron-dependent accumulation of lipid peroxides. Ferroptosis suppressor protein 1 (FSP1) has been shown to work with glutathione peroxidase 4 (GPX4) to suppress ferroptosis through different antioxidant pathways. Many studies have been conducted on FSP1 to better understand its function and mechanism of action, which remained inconclusive in the absence of structural information on FSP1. Recent elucidation of FSP1 structures in different forms and advances in computational characterization of functional changes in its conformation provide us with the opportunity of dissecting FSP1 mechanism of action and gaining insights into critical sites and interactions that control its activity. We present the results from elastic network model analyses of cooperative changes in FSP1 structure, as well as those from molecular dynamics simulations of its interactions with the lipid bilayer and small molecules, toward assisting in future development of modulators of ferroptosis targeting FSP1. Our study reveals the critical role of N-terminal myristoylated tail in modulating the accessibility of the ligand-binding sites and in anchoring FSP1 to the membrane, giving insights into mechanisms of regulating FSP1 function.

摘要

铁死亡是一种细胞死亡形式,其特征是脂质过氧化物依赖铁的积累。铁死亡抑制蛋白1(FSP1)已被证明与谷胱甘肽过氧化物酶4(GPX4)协同作用,通过不同的抗氧化途径抑制铁死亡。为了更好地理解FSP1的功能和作用机制,人们对其进行了许多研究,但在缺乏FSP1结构信息的情况下,这些研究仍无定论。最近对不同形式的FSP1结构的阐明以及对其构象功能变化的计算表征进展,为我们剖析FSP1的作用机制以及深入了解控制其活性的关键位点和相互作用提供了机会。我们展示了FSP1结构协同变化的弹性网络模型分析结果,以及其与脂质双层和小分子相互作用的分子动力学模拟结果,以协助未来针对FSP1的铁死亡调节剂的开发。我们的研究揭示了N端肉豆蔻酰化尾巴在调节配体结合位点的可及性以及将FSP1锚定到膜上的关键作用,从而深入了解调节FSP1功能的机制。

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