• 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

相似文献

1
Sequence divergence in the Treponema denticola FhbB protein and its impact on factor H binding.密螺旋体菌 FhbB 蛋白的序列差异及其对因子 H 结合的影响。
Mol Oral Microbiol. 2013 Aug;28(4):316-30. doi: 10.1111/omi.12027. Epub 2013 Apr 22.
2
Identification of the primary mechanism of complement evasion by the periodontal pathogen, Treponema denticola.鉴定牙周病原体密螺旋体(Treponema denticola)逃避补体的主要机制。
Mol Oral Microbiol. 2011 Apr;26(2):140-9. doi: 10.1111/j.2041-1014.2010.00598.x. Epub 2010 Dec 3.
3
Analysis of the complement sensitivity of oral treponemes and the potential influence of FH binding, FH cleavage and dentilisin activity on the pathogenesis of periodontal disease.分析口腔密螺旋体的补体敏感性以及 FH 结合、FH 裂解和齿龈蛋白酶活性对牙周病发病机制的潜在影响。
Mol Oral Microbiol. 2014 Oct;29(5):194-207. doi: 10.1111/omi.12054. Epub 2014 Jun 3.
4
Analysis of a unique interaction between the complement regulatory protein factor H and the periodontal pathogen Treponema denticola.补体调节蛋白H因子与牙周病原体齿垢密螺旋体之间独特相互作用的分析。
Infect Immun. 2009 Apr;77(4):1417-25. doi: 10.1128/IAI.01544-08. Epub 2009 Feb 9.
5
Development of an FhbB based chimeric vaccinogen that elicits antibodies that block Factor H binding and cleavage by the periopathogen Treponema denticola.基于 FhbB 的嵌合疫苗的开发,可诱导产生抗体,阻断周围病原体密螺旋体牙龈卟啉单胞菌对因子 H 的结合和切割。
Mol Oral Microbiol. 2021 Feb;36(1):50-57. doi: 10.1111/omi.12325. Epub 2020 Dec 9.
6
Plasminogen binding and degradation by Treponema denticola: Identification of the plasminogen binding interface on the FhbB protein.牙龈密螺旋体对纤溶酶原的结合和降解:FhbB 蛋白上纤溶酶原结合界面的鉴定。
Mol Oral Microbiol. 2018 Jun;33(3):249-256. doi: 10.1111/omi.12221. Epub 2018 Apr 23.
7
The Treponema denticola FhbB Protein Is a Dominant Early Antigen That Elicits FhbB Variant-Specific Antibodies That Block Factor H Binding and Cleavage by Dentilisin.齿垢密螺旋体FhbB蛋白是一种主要的早期抗原,可引发FhbB变体特异性抗体,这些抗体可阻断补体因子H与牙蛋白酶的结合及裂解。
Infect Immun. 2016 Jun 23;84(7):2051-2058. doi: 10.1128/IAI.01542-15. Print 2016 Jul.
8
Structure of factor H-binding protein B (FhbB) of the periopathogen, Treponema denticola: insights into progression of periodontal disease.牙周病原体密螺旋体菌(Treponema denticola)中因子 H 结合蛋白 B(FhbB)的结构:对牙周病进展的深入了解。
J Biol Chem. 2012 Apr 13;287(16):12715-22. doi: 10.1074/jbc.M112.339721. Epub 2012 Feb 24.
9
Characterization of the Treponema denticola Virulence Factor Dentilisin.解析:原文是一篇英文论文的标题,需要翻译成中文。“Characterization of the Treponema denticola Virulence Factor Dentilisin.”可直译为“牙龈密螺旋体毒力因子牙龈蛋白酶的特性”。
Methods Mol Biol. 2021;2210:173-184. doi: 10.1007/978-1-0716-0939-2_17.
10
Conservation and revised annotation of the Treponema denticola prcB-prcA-prtP locus encoding the dentilisin (CTLP) protease complex.保守性与 Treponema denticola prcB-prcA-prtP 基因座的重新注释,该基因座编码牙蛋白酶(CTLP)蛋白酶复合物。
Mol Oral Microbiol. 2013 Jun;28(3):181-91. doi: 10.1111/omi.12013. Epub 2012 Dec 17.

引用本文的文献

1
Molecular Analysis of ApiA, a Multi-Functional Protein.多功能蛋白ApiA的分子分析
Pathogens. 2024 Nov 18;13(11):1011. doi: 10.3390/pathogens13111011.
2
Topology and functional characterization of major outer membrane proteins of Treponema maltophilum and Treponema lecithinolyticum.嗜麦芽寡养单胞菌和溶卵磷脂密螺旋体主要外膜蛋白的拓扑结构与功能特性
Mol Oral Microbiol. 2025 Feb;40(1):17-36. doi: 10.1111/omi.12484. Epub 2024 Sep 12.
3
The Treponema denticola FhbB Protein Is a Dominant Early Antigen That Elicits FhbB Variant-Specific Antibodies That Block Factor H Binding and Cleavage by Dentilisin.齿垢密螺旋体FhbB蛋白是一种主要的早期抗原,可引发FhbB变体特异性抗体,这些抗体可阻断补体因子H与牙蛋白酶的结合及裂解。
Infect Immun. 2016 Jun 23;84(7):2051-2058. doi: 10.1128/IAI.01542-15. Print 2016 Jul.
4
The Cross-Talk between Spirochetal Lipoproteins and Immunity.螺旋体脂蛋白与免疫之间的相互作用
Front Immunol. 2014 Jun 30;5:310. doi: 10.3389/fimmu.2014.00310. eCollection 2014.
5
Analysis of the complement sensitivity of oral treponemes and the potential influence of FH binding, FH cleavage and dentilisin activity on the pathogenesis of periodontal disease.分析口腔密螺旋体的补体敏感性以及 FH 结合、FH 裂解和齿龈蛋白酶活性对牙周病发病机制的潜在影响。
Mol Oral Microbiol. 2014 Oct;29(5):194-207. doi: 10.1111/omi.12054. Epub 2014 Jun 3.

本文引用的文献

1
Conservation and revised annotation of the Treponema denticola prcB-prcA-prtP locus encoding the dentilisin (CTLP) protease complex.保守性与 Treponema denticola prcB-prcA-prtP 基因座的重新注释,该基因座编码牙蛋白酶(CTLP)蛋白酶复合物。
Mol Oral Microbiol. 2013 Jun;28(3):181-91. doi: 10.1111/omi.12013. Epub 2012 Dec 17.
2
Structure of factor H-binding protein B (FhbB) of the periopathogen, Treponema denticola: insights into progression of periodontal disease.牙周病原体密螺旋体菌(Treponema denticola)中因子 H 结合蛋白 B(FhbB)的结构:对牙周病进展的深入了解。
J Biol Chem. 2012 Apr 13;287(16):12715-22. doi: 10.1074/jbc.M112.339721. Epub 2012 Feb 24.
3
Treponema denticola interactions with host proteins.齿密螺旋体与宿主蛋白的相互作用。
J Oral Microbiol. 2012;4. doi: 10.3402/jom.v4i0.9929. Epub 2012 Feb 21.
4
Immune evasion strategies of Porphyromonas gingivalis.牙龈卟啉单胞菌的免疫逃避策略
J Oral Biosci. 2011;53(3):233-240. doi: 10.2330/joralbiosci.53.233.
5
Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement.低丰度生物膜物种通过共生菌群和补体来调控炎症性牙周病。
Cell Host Microbe. 2011 Nov 17;10(5):497-506. doi: 10.1016/j.chom.2011.10.006. Epub 2011 Oct 27.
6
Pathogenic microbes and community service through manipulation of innate immunity.致病微生物与通过先天免疫调控实现的社区服务
Adv Exp Med Biol. 2012;946:69-85. doi: 10.1007/978-1-4614-0106-3_5.
7
Crystallization of the factor H-binding protein, FhbB, from the periopathogen Treponema denticola.来自牙周病原体齿垢密螺旋体的因子H结合蛋白FhbB的结晶。
Acta Crystallogr Sect F Struct Biol Cryst Commun. 2011 Jun 1;67(Pt 6):678-81. doi: 10.1107/S1744309111011298. Epub 2011 May 25.
8
Identification of the primary mechanism of complement evasion by the periodontal pathogen, Treponema denticola.鉴定牙周病原体密螺旋体(Treponema denticola)逃避补体的主要机制。
Mol Oral Microbiol. 2011 Apr;26(2):140-9. doi: 10.1111/j.2041-1014.2010.00598.x. Epub 2010 Dec 3.
9
Chronic periodontitis and C-reactive protein levels.慢性牙周炎与 C 反应蛋白水平。
J Periodontol. 2011 Jul;82(7):969-78. doi: 10.1902/jop.2010.100511. Epub 2010 Dec 28.
10
The Treponema denticola chymotrypsin-like protease dentilisin induces matrix metalloproteinase-2-dependent fibronectin fragmentation in periodontal ligament cells.牙龈密螺旋体的糜蛋白酶样蛋白酶牙蛋白酶诱导牙周韧带细胞中基质金属蛋白酶-2 依赖性纤维连接蛋白片段化。
Infect Immun. 2011 Feb;79(2):806-11. doi: 10.1128/IAI.01001-10. Epub 2010 Nov 29.

密螺旋体菌 FhbB 蛋白的序列差异及其对因子 H 结合的影响。

Sequence divergence in the Treponema denticola FhbB protein and its impact on factor H binding.

机构信息

Department of Microbiology and Immunology, Medical College of Virginia at Virginia Commonwealth University, Richmond, VA 23298, USA.

出版信息

Mol Oral Microbiol. 2013 Aug;28(4):316-30. doi: 10.1111/omi.12027. Epub 2013 Apr 22.

DOI:10.1111/omi.12027
PMID:23601078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3785937/
Abstract

Treponema denticola is an anaerobic spirochete whose abundance in the subgingival crevice correlates with the development and severity of periodontal disease. The ability of T. denticola to survive and thrive in the hostile environment of the periodontal pocket is due, at least in part, to its ability to bind factor H (FH), a negative regulator of the alternative complement pathway. The FH binding protein of T. denticola has been identified as FhbB and its atomic structure has been determined. The interaction of FH with T. denticola is unique in that FH bound to the cell surface is cleaved by the T. denticola protease, dentilisin. It has been postulated that FH cleavage by T. denticola leads to immune dysregulation in periodontal pockets. In this study, we conduct a comparative assessment of the sequence, properties, structure and ligand binding kinetics of the FhbB proteins of strains 33521 and 35405. The biological outcome of the interaction of these strains with FH could differ significantly as 33521 lacks dentilisin activity. The data presented here offer insight into our understanding of the interactions of T. denticola with the host and its potential to influence disease progression.

摘要

齿密螺旋体是一种厌氧螺旋体,其在龈下沟中的丰度与牙周病的发展和严重程度相关。齿密螺旋体能够在牙周袋这种恶劣环境中生存和繁殖,这至少部分归因于其能够结合补体途径的负调控因子 FH。齿密螺旋体的 FH 结合蛋白已被鉴定为 FhbB,其原子结构也已被确定。FH 与齿密螺旋体的相互作用是独特的,因为结合到细胞表面的 FH 会被齿密螺旋体蛋白酶 dentilisin 切割。据推测,齿密螺旋体对 FH 的切割会导致牙周袋中的免疫失调。在这项研究中,我们对菌株 33521 和 35405 的 FhbB 蛋白的序列、特性、结构和配体结合动力学进行了比较评估。由于 33521 缺乏 dentilisin 活性,这些菌株与 FH 的相互作用的生物学后果可能会有很大差异。这里呈现的数据为我们理解齿密螺旋体与宿主的相互作用及其影响疾病进展的潜力提供了深入的认识。