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1
Agents that inhibit Rho, Rac, and Cdc42 do not block formation of actin pedestals in HeLa cells infected with enteropathogenic Escherichia coli.抑制Rho、Rac和Cdc42的试剂不会阻断感染肠致病性大肠杆菌的HeLa细胞中肌动蛋白基座的形成。
Infect Immun. 1998 Apr;66(4):1755-8. doi: 10.1128/IAI.66.4.1755-1758.1998.
2
Rho, rac, and cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodia.Rho、rac和cdc42小G蛋白调节与肌动蛋白应力纤维、片状伪足和丝状伪足相关的多分子粘着斑复合体的组装。
Cell. 1995 Apr 7;81(1):53-62. doi: 10.1016/0092-8674(95)90370-4.
3
Rho, rac and cdc42 GTPases: regulators of actin structures, cell adhesion and motility.Rho、Rac和Cdc42小GTP酶：肌动蛋白结构、细胞黏附及运动的调节因子。
Biochem Soc Trans. 1995 Aug;23(3):456-9. doi: 10.1042/bst0230456.
4
The 70 kDa S6 kinase complexes with and is activated by the Rho family G proteins Cdc42 and Rac1.70千道尔顿的S6激酶与Rho家族G蛋白Cdc42和Rac1结合并被其激活。
Cell. 1996 May 17;85(4):573-83. doi: 10.1016/s0092-8674(00)81257-x.
5
Cellularization in Drosophila melanogaster is disrupted by the inhibition of rho activity and the activation of Cdc42 function.在黑腹果蝇中，细胞化过程会因rho活性的抑制和Cdc42功能的激活而受到破坏。
Dev Biol. 1998 Dec 1;204(1):151-64. doi: 10.1006/dbio.1998.9061.
6
Escherichia coli cytotoxic necrotizing factor 1 (CNF1), a toxin that activates the Rho GTPase.大肠杆菌细胞毒素坏死因子1（CNF1），一种激活Rho GTP酶的毒素。
J Biol Chem. 1997 Aug 1;272(31):19532-7. doi: 10.1074/jbc.272.31.19532.
7
Regulation of phosphorylation pathways by p21 GTPases. The p21 Ras-related Rho subfamily and its role in phosphorylation signalling pathways.p21 GTP酶对磷酸化途径的调控。p21 Ras相关的Rho亚家族及其在磷酸化信号通路中的作用。
Eur J Biochem. 1996 Dec 1;242(2):171-85. doi: 10.1111/j.1432-1033.1996.0171r.x.
8
Rho, Rac and Cdc42 GTPases regulate the organization of the actin cytoskeleton.Rho、Rac和Cdc42 GTP酶调节肌动蛋白细胞骨架的组织。
Curr Opin Cell Biol. 1997 Feb;9(1):86-92. doi: 10.1016/s0955-0674(97)80156-1.
9
[Analysis of synaptic neurotransmitter release mechanisms using bacterial toxins].[利用细菌毒素分析突触神经递质释放机制]
J Soc Biol. 1999;193(6):457-67.
10
GTPases of the Rho subfamily are required for Brucella abortus internalization in nonprofessional phagocytes: direct activation of Cdc42.布鲁氏菌（Brucella abortus）在非专职吞噬细胞中内化需要Rho亚家族的GTP酶：Cdc42的直接激活。
J Biol Chem. 2001 Nov 30;276(48):44435-43. doi: 10.1074/jbc.M105606200. Epub 2001 Sep 28.

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1
EPEC Recruits a Cdc42-Specific GEF, Frabin, To Facilitate PAK Activation and Host Cell Colonization.EPEC 通过招募 Cdc42 特异性鸟苷酸交换因子 Frabin 来促进 PAK 的激活和宿主细胞的定植。
mBio. 2020 Nov 3;11(6):e01423-20. doi: 10.1128/mBio.01423-20.
2
Pathogenic Escherichia coli Hijacks GTPase-Activated p21-Activated Kinase for Actin Pedestal Formation.致病性大肠杆菌劫持 GTPase 激活的 p21 激活激酶形成肌动蛋白足。
mBio. 2019 Aug 20;10(4):e01876-19. doi: 10.1128/mBio.01876-19.
3
The Enterohemorrhagic Escherichia coli Effector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner.肠出血性大肠杆菌效应蛋白EspW以Rac1依赖的方式触发肌动蛋白重塑。
Infect Immun. 2017 Aug 18;85(9). doi: 10.1128/IAI.00244-17. Print 2017 Sep.
4
MYO6 is targeted by virulence effectors to trigger PI3-kinase signaling and pathogen invasion into host cells.肌球蛋白 VI（MYO6）被毒力效应物靶向，以触发 PI3-激酶信号传导并使病原体侵入宿主细胞。
Proc Natl Acad Sci U S A. 2017 Apr 11;114(15):3915-3920. doi: 10.1073/pnas.1616418114. Epub 2017 Mar 27.
5
Enteropathogenic Escherichia coli and vaccinia virus do not require the family of WASP-interacting proteins for pathogen-induced actin assembly.肠致病性大肠杆菌和牛痘病毒并不需要 WASP 相互作用蛋白家族来进行病原体诱导的肌动蛋白组装。
Infect Immun. 2012 Dec;80(12):4071-7. doi: 10.1128/IAI.06148-11. Epub 2012 Sep 10.
6
Internalization of Escherichia coli o157:h7 by bovine rectal epithelial cells.牛直肠上皮细胞对大肠杆菌O157:H7的内化作用
Front Microbiol. 2011 Feb 22;2:32. doi: 10.3389/fmicb.2011.00032. eCollection 2011.
7
PKA-mediated phosphorylation of EPEC-Tir at serine residues 434 and 463: A novel pathway in regulating Rac1 GTPase function.蛋白激酶A介导的肠致病性大肠杆菌转位 intimin 受体（EPEC-Tir）丝氨酸残基434和463的磷酸化：调节Rac1 GTP酶功能的新途径。
Gut Microbes. 2010 Mar;1(2):94-99. doi: 10.4161/gmic.1.2.11437. Epub 2010 Feb 8.
8
Structural and functional studies indicate that the EPEC effector, EspG, directly binds p21-activated kinase.结构和功能研究表明，EPEC 效应蛋白 EspG 可直接结合 p21 激活激酶。
Biochemistry. 2011 Feb 15;50(6):917-9. doi: 10.1021/bi1020138. Epub 2011 Jan 24.
9
A bacterial effector targets host DH-PH domain RhoGEFs and antagonizes macrophage phagocytosis.一种细菌效应蛋白靶向宿主 DH-PH 结构域 RhoGEF 并拮抗巨噬细胞吞噬作用。
EMBO J. 2010 Apr 21;29(8):1363-76. doi: 10.1038/emboj.2010.33. Epub 2010 Mar 18.
10
Actin pedestal formation by enteropathogenic Escherichia coli is regulated by IQGAP1, calcium, and calmodulin.肠道致病性大肠杆菌形成肌动蛋白基座受IQGAP1、钙和钙调蛋白调控。
J Biol Chem. 2008 Dec 12;283(50):35212-22. doi: 10.1074/jbc.M803477200. Epub 2008 Sep 22.

本文引用的文献

1
Rho, Rac and Cdc42 GTPases regulate the organization of the actin cytoskeleton.Rho、Rac和Cdc42 GTP酶调节肌动蛋白细胞骨架的组织。
Curr Opin Cell Biol. 1997 Feb;9(1):86-92. doi: 10.1016/s0955-0674(97)80156-1.
2
Attaching and effacing of host cells by enteropathogenic Escherichia coli in the absence of detectable tyrosine kinase mediated signal transduction.在缺乏可检测到的酪氨酸激酶介导的信号转导情况下，致病性大肠杆菌对宿主细胞的黏附和损伤。
Microb Pathog. 1996 Sep;21(3):157-71. doi: 10.1006/mpat.1996.0051.
3
Novel form of actin-based motility transports bacteria on the surfaces of infected cells.基于肌动蛋白的新型运动方式可在受感染细胞表面运输细菌。
Cell Motil Cytoskeleton. 1996;34(4):279-87. doi: 10.1002/(SICI)1097-0169(1996)34:4<279::AID-CM3>3.0.CO;2-3.
4
A pathogenic bacterium triggers epithelial signals to form a functional bacterial receptor that mediates actin pseudopod formation.一种致病细菌触发上皮信号，形成一种功能性细菌受体，该受体介导肌动蛋白伪足的形成。
EMBO J. 1996 Jun 3;15(11):2613-24.
5
The small GTP-binding protein Rho regulates a phosphatidylinositol 4-phosphate 5-kinase in mammalian cells.小GTP结合蛋白Rho在哺乳动物细胞中调节磷脂酰肌醇4-磷酸5-激酶。
Cell. 1994 Nov 4;79(3):507-13. doi: 10.1016/0092-8674(94)90259-3.
6
Improved green fluorescence.增强的绿色荧光。
Nature. 1995 Feb 23;373(6516):663-4. doi: 10.1038/373663b0.
7
Glucosylation of Rho proteins by Clostridium difficile toxin B.艰难梭菌毒素B对Rho蛋白的糖基化作用。
Nature. 1995 Jun 8;375(6531):500-3. doi: 10.1038/375500a0.
8
A genetic locus of enteropathogenic Escherichia coli necessary for the production of attaching and effacing lesions on tissue culture cells.肠道致病性大肠杆菌的一个基因位点，该位点是在组织培养细胞上产生紧密黏附并抹平损伤所必需的。
Proc Natl Acad Sci U S A. 1990 Oct;87(20):7839-43. doi: 10.1073/pnas.87.20.7839.
9
Construction and analysis of TnphoA mutants of enteropathogenic Escherichia coli unable to invade HEp-2 cells.无法侵袭HEp-2细胞的肠致病性大肠杆菌TnphoA突变体的构建与分析
Infect Immun. 1990 Jun;58(6):1565-71. doi: 10.1128/iai.58.6.1565-1571.1990.
10
Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake.肠致病性大肠杆菌（EPEC）与上皮细胞之间的信号转导：EPEC诱导宿主细胞蛋白的酪氨酸磷酸化，以启动细胞骨架重排和细菌摄取。
EMBO J. 1992 Oct;11(10):3551-60. doi: 10.1002/j.1460-2075.1992.tb05438.x.

抑制Rho、Rac和Cdc42的试剂不会阻断感染肠致病性大肠杆菌的HeLa细胞中肌动蛋白基座的形成。

Agents that inhibit Rho, Rac, and Cdc42 do not block formation of actin pedestals in HeLa cells infected with enteropathogenic Escherichia coli.

作者信息

Ben-Ami G, Ozeri V, Hanski E, Hofmann F, Aktories K, Hahn K M, Bokoch G M, Rosenshine I

机构信息

Department of Molecular Genetics and Biotechnology, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.

出版信息

Infect Immun. 1998 Apr;66(4):1755-8. doi: 10.1128/IAI.66.4.1755-1758.1998.

DOI:10.1128/IAI.66.4.1755-1758.1998
PMID:9529109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108116/
Abstract

Enteropathogenic Escherichia coli (EPEC) induces formation of actin pedestals in infected host cells. Agents that inhibit the activity of Rho, Rac, and Cdc42, including Clostridium difficile toxin B (ToxB), compactin, and dominant negative Rho, Rac, and Cdc42, did not inhibit formation of actin pedestals. In contrast, treatment of HeLa cells with ToxB inhibited EPEC invasion. Thus, Rho, Rac, and Cdc42 are not required for assembly of actin pedestals; however, they may be involved in EPEC uptake by HeLa cells.

摘要

肠致病性大肠杆菌（EPEC）可诱导感染的宿主细胞中形成肌动蛋白基座。包括艰难梭菌毒素B（ToxB）、洛伐他汀和显性负性Rho、Rac及Cdc42在内的抑制Rho、Rac和Cdc42活性的试剂，并未抑制肌动蛋白基座的形成。相反，用ToxB处理HeLa细胞可抑制EPEC的侵袭。因此，肌动蛋白基座的组装不需要Rho、Rac和Cdc42；然而，它们可能参与HeLa细胞对EPEC的摄取。