• 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

耶尔森氏菌外膜蛋白:在调节宿主细胞信号转导反应及发病机制中的作用

Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis.

作者信息

Viboud Gloria I, Bliska James B

机构信息

Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, SUNY Stony Brook, Stony Brook, New York 11794-5222, USA.

出版信息

Annu Rev Microbiol. 2005;59:69-89. doi: 10.1146/annurev.micro.59.030804.121320.

DOI:10.1146/annurev.micro.59.030804.121320
PMID:15847602
Abstract

A type III secretion system (TTSS) is encoded on a virulence plasmid that is common to three pathogenic Yersinia species: Y. enterocolitica, Y. pseudotuberculosis, and Y. pestis. Pathogenic Yersinia species require this TTSS to survive and replicate within lymphoid tissues of their animal or human hosts. A set of pathogenicity factors, including those known as Yersinia outer proteins (Yops), is exported by this system upon bacterial infection of host cells. Two translocator Yops (YopB and YopD) insert into the host plasma membrane and function to transport six effector Yops (YopO, YopH, YopM, YopT, YopJ, and YopE) into the cytosol of the host cell. Effector Yops function to counteract multiple signaling responses in the infected host cell. The signaling responses counteracted by Yops are initiated by phagocytic receptors, Toll-like receptors, translocator Yops, and additional mechanisms. Innate and adaptive immune responses are thwarted as a consequence of Yop activities. A biochemical function for each effector Yop has been established, and the importance of these proteins for the pathogenesis process is being elucidated. This review focuses on the biochemical functions of Yops, the signaling pathways they modulate, and the role of these proteins in Yersinia virulence.

摘要

III型分泌系统(TTSS)由一种毒力质粒编码,该质粒在三种致病性耶尔森氏菌中普遍存在,即小肠结肠炎耶尔森氏菌、假结核耶尔森氏菌和鼠疫耶尔森氏菌。致病性耶尔森氏菌需要这种III型分泌系统才能在其动物或人类宿主的淋巴组织内存活和复制。一组致病因子,包括那些被称为耶尔森氏菌外蛋白(Yops)的因子,在细菌感染宿主细胞时由该系统输出。两种转运蛋白Yops(YopB和YopD)插入宿主质膜,并负责将六种效应子Yops(YopO、YopH、YopM、YopT、YopJ和YopE)转运到宿主细胞的细胞质中。效应子Yops的功能是抵消受感染宿主细胞中的多种信号反应。Yops抵消的信号反应由吞噬受体、Toll样受体、转运蛋白Yops和其他机制引发。由于Yop的活性,先天性和适应性免疫反应受到阻碍。已经确定了每种效应子Yop的生化功能,并且这些蛋白质在发病过程中的重要性正在得到阐明。本综述重点关注Yops的生化功能、它们调节的信号通路以及这些蛋白质在耶尔森氏菌毒力中的作用。

相似文献

1
Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis.耶尔森氏菌外膜蛋白:在调节宿主细胞信号转导反应及发病机制中的作用
Annu Rev Microbiol. 2005;59:69-89. doi: 10.1146/annurev.micro.59.030804.121320.
2
Cellular mechanisms of bacterial internalization counteracted by Yersinia.耶尔森氏菌对抗细菌内化的细胞机制。
Int Rev Cytol. 2005;246:135-88. doi: 10.1016/S0074-7696(05)46004-0.
3
Modulation of Rho GTPases and the actin cytoskeleton by Yersinia outer proteins (Yops).耶尔森氏菌外膜蛋白(Yops)对Rho GTP酶和肌动蛋白细胞骨架的调节作用
Int J Med Microbiol. 2001 Sep;291(4):269-76. doi: 10.1078/1438-4221-00130.
4
Analysis of chaperone-dependent Yop secretion/translocation and effector function using a mini-virulence plasmid of Yersinia enterocolitica.利用小肠结肠炎耶尔森氏菌的微型毒力质粒分析伴侣蛋白依赖性Yop分泌/转位及效应子功能。
Int J Med Microbiol. 2003 Jun;293(2-3):167-77. doi: 10.1078/1438-4221-00251.
5
The virulence plasmid of Yersinia, an antihost genome.耶尔森氏菌的毒力质粒,一种抗宿主基因组。
Microbiol Mol Biol Rev. 1998 Dec;62(4):1315-52. doi: 10.1128/MMBR.62.4.1315-1352.1998.
6
Crosstalk of signalling processes of innate immunity with Yersinia Yop effector functions.固有免疫信号传导过程与耶尔森菌Yop效应蛋白功能的相互作用。
Immunobiology. 2008;213(3-4):261-9. doi: 10.1016/j.imbio.2007.11.001. Epub 2007 Dec 31.
7
Contribution of the major secreted yops of Yersinia enterocolitica O:8 to pathogenicity in the mouse infection model.小肠结肠炎耶尔森菌O:8主要分泌性耶尔森菌外膜蛋白(Yops)对小鼠感染模型致病性的贡献
Infect Immun. 2004 Sep;72(9):5227-34. doi: 10.1128/IAI.72.9.5227-5234.2004.
8
The Yersinia Yop virulon: a bacterial system for subverting eukaryotic cells.耶尔森氏菌Yop毒力蛋白分泌系统:一种用于颠覆真核细胞的细菌系统。
Mol Microbiol. 1997 Mar;23(5):861-7. doi: 10.1046/j.1365-2958.1997.2731623.x.
9
The Functions of Effector Proteins in Yersinia Virulence.耶尔森氏菌毒力效应蛋白的功能
Pol J Microbiol. 2016;65(1):5-12. doi: 10.5604/17331331.1197324.
10
Uncovering an Important Role for YopJ in the Inhibition of Caspase-1 in Activated Macrophages and Promoting Yersinia pseudotuberculosis Virulence.揭示YopJ在抑制活化巨噬细胞中半胱天冬酶-1及促进假结核耶尔森菌毒力方面的重要作用。
Infect Immun. 2016 Mar 24;84(4):1062-1072. doi: 10.1128/IAI.00843-15. Print 2016 Apr.

引用本文的文献

1
Characterization and Genome Comparison of Bacteriophage KKU62-1 Infecting Hypervirulent Streptococcus agalactiae ST283.感染高毒力无乳链球菌ST283的噬菌体KKU62-1的特性分析与基因组比较
Curr Microbiol. 2025 Aug 18;82(10):464. doi: 10.1007/s00284-025-04439-z.
2
Characterization of a novel genus bacteriophage and its potential for efficient transfer of modified shuttle plasmids to strains of different clonal complexes.一种新型噬菌体的特性及其将修饰的穿梭质粒高效转移至不同克隆复合体菌株的潜力。
Microbiol Spectr. 2025 Jul 11:e0333224. doi: 10.1128/spectrum.03332-24.
3
Yersinia pseudotuberculosis growth arrest during type-III secretion system expression is associated with altered ribosomal protein expression and decreased gentamicin susceptibility.
Ⅲ型分泌系统表达期间假结核耶尔森菌的生长停滞与核糖体蛋白表达改变及庆大霉素敏感性降低有关。
PLoS Pathog. 2025 Jul 7;21(7):e1012548. doi: 10.1371/journal.ppat.1012548. eCollection 2025 Jul.
4
Population structure and gene flux of ST121 reveal prophages as a candidate driver of adaptation and persistence in food production environments.ST121的种群结构和基因流动揭示了前噬菌体是食品生产环境中适应性和持久性的候选驱动因素。
Microb Genom. 2025 Apr;11(4). doi: 10.1099/mgen.0.001397.
5
Type III Secretion System in Intestinal Pathogens and Metabolic Diseases.肠道病原体与代谢疾病中的 III 型分泌系统。
J Diabetes Res. 2024 Nov 6;2024:4864639. doi: 10.1155/2024/4864639. eCollection 2024.
6
Distinct mechanisms of type 3 secretion system recognition control LTB4 synthesis in neutrophils and macrophages.3 型分泌系统识别的不同机制控制中性粒细胞和巨噬细胞中 LTB4 的合成。
PLoS Pathog. 2024 Oct 18;20(10):e1012651. doi: 10.1371/journal.ppat.1012651. eCollection 2024 Oct.
7
growth arrest during type-III secretion system expression is associated with altered ribosomal protein expression and decreased gentamicin susceptibility.III型分泌系统表达期间的生长停滞与核糖体蛋白表达改变和庆大霉素敏感性降低有关。
bioRxiv. 2024 Sep 2:2024.09.02.610769. doi: 10.1101/2024.09.02.610769.
8
Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages.抑制 IKK 信号转导诱导人巨噬细胞发生 RIPK1 非依赖性细胞凋亡。
PLoS Pathog. 2024 Aug 26;20(8):e1012469. doi: 10.1371/journal.ppat.1012469. eCollection 2024 Aug.
9
Non-canonical autophosphorylation of RIPK1 drives timely pyroptosis to control Yersinia infection.非规范的 RIPK1 自身磷酸化驱动适时细胞焦亡以控制耶尔森菌感染。
Cell Rep. 2024 Aug 27;43(8):114641. doi: 10.1016/j.celrep.2024.114641. Epub 2024 Aug 17.
10
A protein O-GlcNAc glycosyltransferase regulates the antioxidative response in Yersinia pestis.一种蛋白质 O-GlcNAc 糖基转移酶调节鼠疫耶尔森氏菌的抗氧化反应。
Nat Commun. 2024 Aug 16;15(1):7062. doi: 10.1038/s41467-024-50959-w.