SARS-CoV-2 spike and its adaptable furin cleavage site.
作者信息
Whittaker Gary R
机构信息
College of Veterinary Medicine and Public Health Program, Cornell University, Ithaca, NY 14853, USA.
出版信息
Lancet Microbe. 2021 Oct;2(10):e488-e489. doi: 10.1016/S2666-5247(21)00174-9. Epub 2021 Aug 6.
Abstract
摘要
相似文献
1
SARS-CoV-2 spike and its adaptable furin cleavage site.严重急性呼吸综合征冠状病毒2（SARS-CoV-2）刺突蛋白及其适应性弗林蛋白酶切割位点
Lancet Microbe. 2021 Oct;2(10):e488-e489. doi: 10.1016/S2666-5247(21)00174-9. Epub 2021 Aug 6.
2
D614G Substitution of SARS-CoV-2 Spike Protein Increases Syncytium Formation and Virus Titer via Enhanced Furin-Mediated Spike Cleavage.SARS-CoV-2 刺突蛋白 D614G 取代增加合胞体形成和病毒滴度通过增强的弗林蛋白酶介导的刺突裂解。
mBio. 2021 Aug 31;12(4):e0058721. doi: 10.1128/mBio.00587-21. Epub 2021 Jul 27.
3
Loss of furin cleavage site attenuates SARS-CoV-2 pathogenesis.去除furin 酶切位点可减轻 SARS-CoV-2 的发病机制。
Nature. 2021 Mar;591(7849):293-299. doi: 10.1038/s41586-021-03237-4. Epub 2021 Jan 25.
4
The furin cleavage site in the SARS-CoV-2 spike protein is required for transmission in ferrets.SARS-CoV-2 刺突蛋白中的弗林裂解位点是在雪貂中传播所必需的。
Nat Microbiol. 2021 Jul;6(7):899-909. doi: 10.1038/s41564-021-00908-w. Epub 2021 Apr 27.
5
SARS-CoV-2 Bearing a Mutation at the S1/S2 Cleavage Site Exhibits Attenuated Virulence and Confers Protective Immunity.SARS-CoV-2 携带 S1/S2 裂解位点突变表现出毒力减弱，并赋予保护性免疫。
mBio. 2021 Aug 31;12(4):e0141521. doi: 10.1128/mBio.01415-21. Epub 2021 Aug 24.
6
The SARS-CoV-2 Transcriptome and the Dynamics of the S Gene Furin Cleavage Site in Primary Human Airway Epithelia.严重急性呼吸综合征冠状病毒2（SARS-CoV-2）转录组及人原代气道上皮细胞中S基因弗林蛋白酶切割位点的动态变化
mBio. 2021 May 11;12(3):e01006-21. doi: 10.1128/mBio.01006-21.
7
Proteolytic Activation of SARS-CoV-2 Spike at the S1/S2 Boundary: Potential Role of Proteases beyond Furin.SARS-CoV-2 刺突蛋白在 S1/S2 边界处的蛋白水解激活：除弗林蛋白酶以外的蛋白酶的潜在作用。
ACS Infect Dis. 2021 Feb 12;7(2):264-272. doi: 10.1021/acsinfecdis.0c00701. Epub 2021 Jan 12.
8
Propagation of SARS-CoV-2 in Calu-3 Cells to Eliminate Mutations in the Furin Cleavage Site of Spike.在 Calu-3 细胞中传播 SARS-CoV-2 以消除刺突中弗林裂解位点的突变。
Viruses. 2021 Dec 4;13(12):2434. doi: 10.3390/v13122434.
9
Characterisation of the transcriptome and proteome of SARS-CoV-2 reveals a cell passage induced in-frame deletion of the furin-like cleavage site from the spike glycoprotein.对 SARS-CoV-2 的转录组和蛋白质组进行了特征描述，发现刺突糖蛋白上的弗林样裂解位点发生了细胞传代诱导的框内缺失。
Genome Med. 2020 Jul 28;12(1):68. doi: 10.1186/s13073-020-00763-0.
10
QTQTN motif upstream of the furin-cleavage site plays a key role in SARS-CoV-2 infection and pathogenesis.furin 切割位点上游的 QTQTN 基序在 SARS-CoV-2 感染和发病机制中起关键作用。
Proc Natl Acad Sci U S A. 2022 Aug 9;119(32):e2205690119. doi: 10.1073/pnas.2205690119. Epub 2022 Jul 26.
引用本文的文献
1
The Binding of Brazilin from to the Full-Length SARS-CoV-2 Spike Proteins.来自[具体来源]的巴西苏木素与全长严重急性呼吸综合征冠状病毒2刺突蛋白的结合。
Int J Mol Sci. 2025 Apr 25;26(9):4100. doi: 10.3390/ijms26094100.
2
Allosteric modulation by the fatty acid site in the glycosylated SARS-CoV-2 spike.糖基化的严重急性呼吸综合征冠状病毒2（SARS-CoV-2）刺突蛋白中脂肪酸位点的变构调节
Elife. 2025 Apr 10;13:RP97313. doi: 10.7554/eLife.97313.
3
Allosteric Control and Glycan Shielding Adaptations in the SARS-CoV-2 Spike from Early to Peak Virulence.从早期到峰值毒力阶段，严重急性呼吸综合征冠状病毒2（SARS-CoV-2）刺突蛋白的变构调控与聚糖屏蔽适应性
bioRxiv. 2025 Mar 12:2025.03.11.642723. doi: 10.1101/2025.03.11.642723.
4
Role of furin in the severity of COVID-19 infection via effects on miR-20b and miR-106a.弗林蛋白酶通过对miR-20b和miR-106a的影响在新冠病毒感染严重程度中的作用
Mol Biol Rep. 2025 Mar 17;52(1):320. doi: 10.1007/s11033-025-10340-6.
5
Leveraging Artificial Intelligence and Gene Expression Analysis to Identify Some Potential Bovine Coronavirus (BCoV) Receptors and Host Cell Enzymes Potentially Involved in the Viral Replication and Tissue Tropism.利用人工智能和基因表达分析来鉴定一些潜在的牛冠状病毒（BCoV）受体以及可能参与病毒复制和组织嗜性的宿主细胞酶。
Int J Mol Sci. 2025 Feb 4;26(3):1328. doi: 10.3390/ijms26031328.
6
Coordination chemistry suggests that independently observed benefits of metformin and Zn against COVID-19 are not independent.配位化学表明，二甲双胍和锌对新冠病毒独立观察到的益处并非相互独立。
Biometals. 2024 Aug;37(4):983-1022. doi: 10.1007/s10534-024-00590-5. Epub 2024 Apr 5.
7
Differentiating Cell Entry Potentials of SARS-CoV-2 Omicron Subvariants on Human Lung Epithelium Cells.区分 SARS-CoV-2 奥密克戎亚变种对人肺上皮细胞的细胞进入潜力。
Viruses. 2024 Mar 1;16(3):391. doi: 10.3390/v16030391.
8
Comparison of SARS-CoV-2 variants of concern in primary human nasal cultures demonstrates Delta as most cytopathic and Omicron as fastest replicating.在原代人鼻腔培养物中比较关注的 SARS-CoV-2 变异株，表明德尔塔变异株具有最高的细胞病变效应，而奥密克戎变异株复制速度最快。
mBio. 2024 Apr 10;15(4):e0312923. doi: 10.1128/mbio.03129-23. Epub 2024 Mar 13.
9
Biophysical Analysis of Potential Inhibitors of SARS-CoV-2 Cell Recognition and Their Effect on Viral Dynamics in Different Cell Types: A Computational Prediction from In Vitro Experimental Data.严重急性呼吸综合征冠状病毒2（SARS-CoV-2）细胞识别潜在抑制剂的生物物理分析及其对不同细胞类型中病毒动力学的影响：基于体外实验数据的计算预测
ACS Omega. 2024 Feb 14;9(8):8923-8939. doi: 10.1021/acsomega.3c06968. eCollection 2024 Feb 27.
10
Causes and Consequences of Coronavirus Spike Protein Variability.冠状病毒刺突蛋白变异性的原因和后果。
Viruses. 2024 Jan 25;16(2):177. doi: 10.3390/v16020177.
本文引用的文献
1
Functional evaluation of the P681H mutation on the proteolytic activation of the SARS-CoV-2 variant B.1.1.7 (Alpha) spike.P681H突变对严重急性呼吸综合征冠状病毒2变异株B.1.1.7（阿尔法）刺突蛋白的蛋白水解激活的功能评估。
iScience. 2022 Jan 21;25(1):103589. doi: 10.1016/j.isci.2021.103589. Epub 2021 Dec 10.
2
Coronavirus entry: how we arrived at SARS-CoV-2.冠状病毒进入机制：我们如何了解到 SARS-CoV-2。
Curr Opin Virol. 2021 Apr;47:113-120. doi: 10.1016/j.coviro.2021.02.006. Epub 2021 Mar 9.
3
Proteolytic Activation of SARS-CoV-2 Spike at the S1/S2 Boundary: Potential Role of Proteases beyond Furin.SARS-CoV-2 刺突蛋白在 S1/S2 边界处的蛋白水解激活：除弗林蛋白酶以外的蛋白酶的潜在作用。
ACS Infect Dis. 2021 Feb 12;7(2):264-272. doi: 10.1021/acsinfecdis.0c00701. Epub 2021 Jan 12.
4
The proximal origin of SARS-CoV-2.严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的近端起源。
Nat Med. 2020 Apr;26(4):450-452. doi: 10.1038/s41591-020-0820-9.
5
Coronavirus Spike Protein and Tropism Changes.冠状病毒刺突蛋白与嗜性变化
Adv Virus Res. 2016;96:29-57. doi: 10.1016/bs.aivir.2016.08.004. Epub 2016 Sep 13.
6
Insertion of a multibasic cleavage site in the haemagglutinin of human influenza H3N2 virus does not increase pathogenicity in ferrets.插入一个多碱性裂解位点并不会增加人季节性 H3N2 流感病毒在雪貂中的致病性。
J Gen Virol. 2011 Jun;92(Pt 6):1410-1415. doi: 10.1099/vir.0.030379-0. Epub 2011 Feb 23.
7
Recombination, reservoirs, and the modular spike: mechanisms of coronavirus cross-species transmission.重组、宿主和模块化刺突：冠状病毒跨物种传播的机制。
J Virol. 2010 Apr;84(7):3134-46. doi: 10.1128/JVI.01394-09. Epub 2009 Nov 11.
8
Furin at the cutting edge: from protein traffic to embryogenesis and disease.弗林蛋白酶处于前沿：从蛋白质运输到胚胎发育及疾病
Nat Rev Mol Cell Biol. 2002 Oct;3(10):753-66. doi: 10.1038/nrm934.
9
Role of hemagglutinin cleavage for the pathogenicity of influenza virus.血凝素裂解对流感病毒致病性的作用。
Virology. 1999 May 25;258(1):1-20. doi: 10.1006/viro.1999.9716.
Zotero 插件