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Involvement of Ras-related Rho proteins in the mechanisms of action of Clostridium difficile toxin A and toxin B.Ras相关的Rho蛋白在艰难梭菌毒素A和毒素B作用机制中的参与情况。
Infect Immun. 1995 Apr;63(4):1421-6. doi: 10.1128/iai.63.4.1421-1426.1995.
2
The low molecular mass GTP-binding protein Rho is affected by toxin A from Clostridium difficile.低分子量GTP结合蛋白Rho受艰难梭菌毒素A的影响。
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Transient expression of RhoA, -B, and -C GTPases in HeLa cells potentiates resistance to Clostridium difficile toxins A and B but not to Clostridium sordellii lethal toxin.RhoA、-B和-C GTP酶在HeLa细胞中的瞬时表达增强了对艰难梭菌毒素A和B的抗性，但对索氏梭菌致死毒素没有抗性。
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本文引用的文献

1
Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
2
A novel role for RhoGDI as an inhibitor of GAP proteins.Rho鸟苷酸解离抑制蛋白作为GAP蛋白抑制剂的新作用。
EMBO J. 1993 May;12(5):1915-21. doi: 10.1002/j.1460-2075.1993.tb05840.x.
3
Ly-GDI, a GDP-dissociation inhibitor of the RhoA GTP-binding protein, is expressed preferentially in lymphocytes.淋巴细胞特异性鸟苷酸解离抑制剂（Ly-GDI）是一种RhoA GTP结合蛋白的GDP解离抑制剂，在淋巴细胞中优先表达。
Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7568-72. doi: 10.1073/pnas.90.16.7568.
4
Activation of platelet phosphatidylinositide 3-kinase requires the small GTP-binding protein Rho.血小板磷脂酰肌醇3激酶的激活需要小GTP结合蛋白Rho。
J Biol Chem. 1993 Oct 25;268(30):22251-4.
5
Cytotoxic necrotizing factor type 2 produced by virulent Escherichia coli modifies the small GTP-binding proteins Rho involved in assembly of actin stress fibers.由致病性大肠杆菌产生的细胞毒性坏死因子2可修饰参与肌动蛋白应激纤维组装的小GTP结合蛋白Rho。
Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3814-8. doi: 10.1073/pnas.91.9.3814.
6
Clostridium difficile toxin B acts on the GTP-binding protein Rho.艰难梭菌毒素B作用于GTP结合蛋白Rho。
J Biol Chem. 1994 Apr 8;269(14):10706-12.
7
Clostridium difficile colitis.艰难梭菌结肠炎
N Engl J Med. 1994 Jan 27;330(4):257-62. doi: 10.1056/NEJM199401273300406.
8
Probing the action of Clostridium difficile toxin B in Xenopus laevis oocytes.探究艰难梭菌毒素B在非洲爪蟾卵母细胞中的作用。
J Cell Sci. 1994 Jun;107 ( Pt 6):1653-9. doi: 10.1242/jcs.107.6.1653.
9
Comparison of two toxins produced by Clostridium difficile.艰难梭菌产生的两种毒素的比较。
Infect Immun. 1981 Dec;34(3):1036-43. doi: 10.1128/iai.34.3.1036-1043.1981.
10
Ultrastructural effects of Clostridium difficile toxin B on smooth muscle cells and fibroblasts.艰难梭菌毒素B对平滑肌细胞和成纤维细胞的超微结构影响
Exp Cell Res. 1983 Oct 15;148(2):413-22. doi: 10.1016/0014-4827(83)90163-5.

Ras相关的Rho蛋白在艰难梭菌毒素A和毒素B作用机制中的参与情况。

Involvement of Ras-related Rho proteins in the mechanisms of action of Clostridium difficile toxin A and toxin B.

作者信息

Dillon S T, Rubin E J, Yakubovich M, Pothoulakis C, LaMont J T, Feig L A, Gilbert R J

机构信息

Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts 02111.

出版信息

Infect Immun. 1995 Apr;63(4):1421-6. doi: 10.1128/iai.63.4.1421-1426.1995.

DOI:10.1128/iai.63.4.1421-1426.1995
PMID:7890404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173169/
Abstract

Toxins A and B of Clostridium difficile are responsible for pseudomembranous colitis, a disease that afflicts a substantial number of hospitalized patients treated with antibiotics. A major effect of these proteins is the disruption of the actin cytoskeleton. Recently, I. Just, G. Fritz, K. Aktories, M. Giry, M. R. Popoff, P. Boquet, S. Hegenbarth, and C. von Eichel-Streiber (J. Biol. Chem. 269:10706-10712, 1994) implicated Rho proteins as cellular targets of C. difficile toxin B, since pretreatment of cells or purified Rho with toxin prevented subsequent ADP-ribosylation of Rho by exoenzyme C3. Moreover, they showed that overexpression of Rho proteins in cells suppressed cell rounding normally associated with exposure of cells to C. difficile toxin B. Here we expand these findings by showing directly that Rho proteins are covalently modified by both C. difficile toxins A and B. In addition, we demonstrate that the stability of toxin-modified Rho in NIH 3T3 cells is dramatically reduced. Finally, we show that C. difficile toxins A and B do not have similar effects on the closely related Rac and CDC42 GTP-binding proteins.

摘要

艰难梭菌的毒素A和B会引发假膜性结肠炎，这种疾病折磨着大量接受抗生素治疗的住院患者。这些蛋白质的一个主要作用是破坏肌动蛋白细胞骨架。最近，I. 贾斯特、G. 弗里茨、K. 阿克托里斯、M. 吉里、M. R. 波普夫、P. 博凯、S. 黑根巴思和C. 冯·艾歇尔 - 施特雷伯（《生物化学杂志》269:10706 - 10712，1994年）指出Rho蛋白是艰难梭菌毒素B的细胞靶点，因为用毒素对细胞或纯化的Rho进行预处理可阻止随后外切酶C3对Rho的ADP核糖基化。此外，他们表明细胞中Rho蛋白的过表达抑制了通常与细胞暴露于艰难梭菌毒素B相关的细胞变圆现象。在此，我们通过直接证明Rho蛋白被艰难梭菌毒素A和B共价修饰来扩展这些发现。此外，我们证明在NIH 3T3细胞中毒素修饰的Rho的稳定性显著降低。最后，我们表明艰难梭菌毒素A和B对密切相关的Rac和CDC42 GTP结合蛋白没有类似的作用。