• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

基于结构的tau磷酸化激酶DYRK1A抑制剂的发现,用于神经炎症性疾病的治疗靶点:来自微秒级分子动力学模拟和MMPBSA分析的见解

Structure-guided discovery of tau-phosphorylating kinase DYRK1A inhibitors for therapeutic targeting of neuroinflammatory diseases: Insights from microsecond MD simulation and MMPBSA analyses.

作者信息

Choudhury Arunabh, Khan Sumaiya, Saeed Mohammad Umar, Mohammad Taj, Hussain Afzal, AlAjmi Mohamed F, Fatima Urooj, Islam Asimul, Hassan Md Imtaiyaz

机构信息

Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, New Delhi, 110025, India.

Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.

出版信息

Biochem Biophys Res Commun. 2025 Aug 15;775:152166. doi: 10.1016/j.bbrc.2025.152166. Epub 2025 Jun 8.

DOI:10.1016/j.bbrc.2025.152166
PMID:40505550
Abstract

Tauopathies are a class of nearly 20 neurodegenerative diseases, classified into primary and secondary tauopathies. Alzheimer's disease (AD) is a type of secondary tauopathy in which abnormal phosphorylation of tau proteins takes place, which is linked to the kinase activity of dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A). Overexpression of DYRK1A hyperphosphorylates the tau protein, leading to its aggregation. Inhibiting DYRK1A activity can be a promising strategy to prevent tau hyperphosphorylation. In this study, we conducted a virtual screening of natural bioactive compounds from the ZINC database to identify potential small-molecule inhibitors of DYRK1A. The analyses revealed two compounds, ZINC08300244 and ZINC08964763, which showed a high binding affinity with DYRK1A and appropriate pharmacokinetic properties. Density functional theory (DFT) analysis of these two compounds was performed, and their stability of interaction with DYRK1A was further analysed by all-atom molecular dynamics (MD) simulations for 1 μs. Analysis of the MD trajectories was also performed using MM/PBSA and per-residue binding free energy decomposition. The results indicated the stable complex formation of DYRK1A with the two selected molecules for DYRK1A inhibition to prevent tau-hyperphosphorylation. This study highlights the use of virtual screening and MD simulations in finding natural product-based inhibitors of DYRK1A, which may lead to the development of novel therapeutic strategies for treating neuroinflammatory diseases.

摘要

tau蛋白病是一类近20种神经退行性疾病,分为原发性和继发性tau蛋白病。阿尔茨海默病(AD)是一种继发性tau蛋白病,其中tau蛋白发生异常磷酸化,这与双特异性酪氨酸磷酸化调节激酶1A(DYRK1A)的激酶活性有关。DYRK1A的过表达使tau蛋白过度磷酸化,导致其聚集。抑制DYRK1A活性可能是预防tau蛋白过度磷酸化的一种有前景的策略。在本研究中,我们对ZINC数据库中的天然生物活性化合物进行了虚拟筛选,以鉴定DYRK1A的潜在小分子抑制剂。分析发现了两种化合物,ZINC08300244和ZINC08964763,它们与DYRK1A表现出高结合亲和力和合适的药代动力学性质。对这两种化合物进行了密度泛函理论(DFT)分析,并通过全原子分子动力学(MD)模拟1 μs进一步分析了它们与DYRK1A相互作用的稳定性。还使用MM/PBSA和每个残基的结合自由能分解对MD轨迹进行了分析。结果表明,DYRK1A与两种选定分子形成稳定的复合物,可抑制DYRK1A以防止tau蛋白过度磷酸化。本研究强调了虚拟筛选和MD模拟在寻找基于天然产物的DYRK1A抑制剂中的应用,这可能会导致开发治疗神经炎症性疾病的新治疗策略。

相似文献

1
Structure-guided discovery of tau-phosphorylating kinase DYRK1A inhibitors for therapeutic targeting of neuroinflammatory diseases: Insights from microsecond MD simulation and MMPBSA analyses.基于结构的tau磷酸化激酶DYRK1A抑制剂的发现,用于神经炎症性疾病的治疗靶点:来自微秒级分子动力学模拟和MMPBSA分析的见解
Biochem Biophys Res Commun. 2025 Aug 15;775:152166. doi: 10.1016/j.bbrc.2025.152166. Epub 2025 Jun 8.
2
Unlocking the Therapeutic Potential of the Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A Inhibitors in Alzheimer's Diseases.揭示双特异性酪氨酸磷酸化调节激酶1A抑制剂在阿尔茨海默病中的治疗潜力
Mol Neurobiol. 2025 Mar 5. doi: 10.1007/s12035-025-04806-8.
3
Targeting tau hyperphosphorylation-mediated neuroinflammation in Alzheimer's disease via ABL1 kinase inhibition: Insights from microsecond MD simulation and MM/PBSA analyses.通过抑制ABL1激酶靶向阿尔茨海默病中tau蛋白过度磷酸化介导的神经炎症:微秒级分子动力学模拟和MM/PBSA分析的见解
Int J Biol Macromol. 2025 Aug;320(Pt 2):145785. doi: 10.1016/j.ijbiomac.2025.145785. Epub 2025 Jul 5.
4
Unlocking the Conformational Secrets of DYRK1A Kinase With Computational Microscope: Exploring Phosphorylation-Driven Structural Dynamics.用计算显微镜揭示DYRK1A激酶的构象奥秘:探索磷酸化驱动的结构动力学
J Comput Chem. 2025 Jun 30;46(17):e70172. doi: 10.1002/jcc.70172.
5
Integrative machine learning and molecular simulation approaches identify GSK3β inhibitors for neurodegenerative disease therapy.整合机器学习和分子模拟方法鉴定用于神经退行性疾病治疗的糖原合成酶激酶3β抑制剂。
Sci Rep. 2025 Jul 1;15(1):21632. doi: 10.1038/s41598-025-04129-7.
6
[I]IPPI for Tau Imaging: Binding Studies in Postmortem Human Alzheimer's Disease Hippocampus-Subiculum and Evaluation of Drug Effects.[I]用于tau成像的IPPI:对死后人类阿尔茨海默病海马-下托的结合研究及药物效果评估。
Synapse. 2025 Jul;79(4):e70024. doi: 10.1002/syn.70024.
7
Exploring Type II Diabetes Inhibitors from Genus Daphne Plant-species: An Integrated Computational Study.探索瑞香属植物物种中的II型糖尿病抑制剂:一项综合计算研究。
Comb Chem High Throughput Screen. 2025;28(8):1413-1442. doi: 10.2174/0113862073262227231005074024.
8
Towards Imaging Tau Hyperphosphorylation: Is DYRK1A a Potential Target for Imaging Hyperphosphorylation of Tau? Molecular Modeling Assessment and Synthesis of [I]Radioiodinated DYRK1A Inhibitor.迈向tau蛋白过度磷酸化成像:双重特异性酪氨酸磷酸化调节激酶1A(DYRK1A)是tau蛋白过度磷酸化成像的潜在靶点吗?分子建模评估与放射性碘化DYRK1A抑制剂的合成
Molecules. 2025 Feb 21;30(5):990. doi: 10.3390/molecules30050990.
9
Discovery of a novel chemotype as DYRK1A inhibitors against Alzheimer's disease: Computational modeling and biological evaluation.发现一种新型化学型作为 DYRK1A 抑制剂用于治疗阿尔茨海默病:计算建模与生物学评价。
Int J Biol Macromol. 2024 Jun;269(Pt 1):132024. doi: 10.1016/j.ijbiomac.2024.132024. Epub 2024 May 3.
10
Targeting Cyclin-Dependent Kinase 12 (CDK12) for Cancer Therapy: Structure-Based Discovery of Two Novel CDK12 Inhibitors Using Integrated Bioinformatics.靶向细胞周期蛋白依赖性激酶12(CDK12)用于癌症治疗:基于结构利用综合生物信息学发现两种新型CDK12抑制剂
OMICS. 2025 Jul;29(7):341-351. doi: 10.1089/omi.2025.0060. Epub 2025 Jun 13.