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通过氢/氘交换质谱法揭示的CNOT1(800 - 999) HEAT结构域及其与锌指蛋白(TTP)的相互作用

Exploring the CNOT1(800-999) HEAT Domain and Its Interactions with Tristetraprolin (TTP) as Revealed by Hydrogen/Deuterium Exchange Mass Spectrometry.

作者信息

Cieplak-Rotowska Maja K, Dadlez Michał, Niedzwiecka Anna

机构信息

Division of Biophysics, Institute of Experimental Physics, Faculty of Physics, University of Warsaw, PL-02089 Warsaw, Poland.

Laboratory of Biological Physics, Institute of Physics, Polish Academy of Sciences, Aleja Lotnikow 32/46, PL-02668 Warsaw, Poland.

出版信息

Biomolecules. 2025 Mar 11;15(3):403. doi: 10.3390/biom15030403.

Abstract

CNOT1, a key scaffold in the CCR4-NOT complex, plays a critical role in mRNA decay, particularly in the regulation of inflammatory responses through its interaction with tristetraprolin. A fragment of the middle part of CNOT1 (residues 800-999) is an example of an α-helical HEAT-like repeat domain. The HEAT motif is an evolutionarily conserved motif present in scaffolding and transport proteins across a wide range of organisms. Using hydrogen/deuterium exchange mass spectrometry (HDX MS), a method that has not been widely explored in the context of HEAT repeats, we analysed the structural dynamics of wild-type CNOT1(800-999) and its two double point mutants (E893A/Y900A, E893Q/Y900H) to find the individual contributions of these CNOT1 residues to the molecular recognition of tristetraprolin (TTP). Our results show that the differences in the interactions of CNOT1(800-999) variants with the TTP peptide fragment are due to the absence of the critical residues resulting from point mutations and not due to the perturbation of the protein structure. Nevertheless, the HDX MS was able to detect slight local changes in structural dynamics induced by protein point mutations, which are usually neglected in studies of intermolecular interactions.

摘要

CNOT1是CCR4 - NOT复合物中的关键支架蛋白,在mRNA降解中起关键作用,特别是通过与锌指蛋白Tristetraprolin相互作用来调节炎症反应。CNOT1中部的一个片段(800 - 999位氨基酸残基)是α - 螺旋HEAT样重复结构域的一个例子。HEAT基序是一种在广泛生物体的支架蛋白和转运蛋白中存在的进化保守基序。我们使用氢/氘交换质谱法(HDX MS)(一种在HEAT重复序列背景下尚未广泛探索的方法)分析了野生型CNOT1(800 - 999)及其两个双点突变体(E893A/Y900A、E893Q/Y900H)的结构动力学,以确定这些CNOT1残基对锌指蛋白Tristetraprolin(TTP)分子识别的各自贡献。我们的结果表明,CNOT1(800 - 999)变体与TTP肽片段相互作用的差异是由于点突变导致关键残基缺失,而非蛋白质结构的扰动。尽管如此,HDX MS能够检测到蛋白质点突变引起的结构动力学轻微局部变化,而这些变化在分子间相互作用研究中通常被忽略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f4b/11939966/f37c294a7b6d/biomolecules-15-00403-g001.jpg

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