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Journal Abstract Search

164 related items for PubMed ID: 9327754

  • 1. Bacterial toxins block endothelial wound repair. Evidence that Rho GTPases control cytoskeletal rearrangements in migrating endothelial cells.
    Aepfelbacher M, Essler M, Huber E, Sugai M, Weber PC.
    Arterioscler Thromb Vasc Biol; 1997 Sep; 17(9):1623-9. PubMed ID: 9327754
    [Abstract] [Full Text] [Related]

  • 2. Rho proteins play a critical role in cell migration during the early phase of mucosal restitution.
    Santos MF, McCormack SA, Guo Z, Okolicany J, Zheng Y, Johnson LR, Tigyi G.
    J Clin Invest; 1997 Jul 01; 100(1):216-25. PubMed ID: 9202074
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  • 3. Effects of cytotoxic necrotizing factor 1 and lethal toxin on actin cytoskeleton and VE-cadherin localization in human endothelial cell monolayers.
    Vouret-Craviari V, Grall D, Flatau G, Pouysségur J, Boquet P, Van Obberghen-Schilling E.
    Infect Immun; 1999 Jun 01; 67(6):3002-8. PubMed ID: 10338511
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  • 5. Monocyte adhesion and spreading on human endothelial cells is dependent on Rho-regulated receptor clustering.
    Wójciak-Stothard B, Williams L, Ridley AJ.
    J Cell Biol; 1999 Jun 14; 145(6):1293-307. PubMed ID: 10366600
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  • 6. Involvement of rho p21 in cyclic strain-induced tyrosine phosphorylation of focal adhesion kinase (pp125FAK), morphological changes and migration of endothelial cells.
    Yano Y, Saito Y, Narumiya S, Sumpio BE.
    Biochem Biophys Res Commun; 1996 Jul 16; 224(2):508-15. PubMed ID: 8702419
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  • 7. Bordetella bronchiseptica dermonecrotizing toxin stimulates assembly of actin stress fibers and focal adhesions by modifying the small GTP-binding protein rho.
    Horiguchi Y, Senda T, Sugimoto N, Katahira J, Matsuda M.
    J Cell Sci; 1995 Oct 16; 108 ( Pt 10)():3243-51. PubMed ID: 7593285
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  • 8. Rho and Rac exert antagonistic functions on spreading of macrophage-derived multinucleated cells and are not required for actin fiber formation.
    Ory S, Munari-Silem Y, Fort P, Jurdic P.
    J Cell Sci; 2000 Apr 16; 113 ( Pt 7)():1177-88. PubMed ID: 10704369
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  • 9. Endothelial Rho signaling is required for monocyte transendothelial migration.
    Strey A, Janning A, Barth H, Gerke V.
    FEBS Lett; 2002 Apr 24; 517(1-3):261-6. PubMed ID: 12062449
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  • 10. Clostridial ADP-ribosylating toxins: effects on ATP and GTP-binding proteins.
    Aktories K.
    Mol Cell Biochem; 1994 Sep 24; 138(1-2):167-76. PubMed ID: 7898461
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  • 12. Regulation of TNF-alpha-induced reorganization of the actin cytoskeleton and cell-cell junctions by Rho, Rac, and Cdc42 in human endothelial cells.
    Wójciak-Stothard B, Entwistle A, Garg R, Ridley AJ.
    J Cell Physiol; 1998 Jul 24; 176(1):150-65. PubMed ID: 9618155
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  • 14. RhoA inactivation enhances endothelial barrier function.
    Carbajal JM, Schaeffer RC.
    Am J Physiol; 1999 Nov 24; 277(5 Pt 1):C955-64. PubMed ID: 10564088
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  • 15. Clostridium difficile toxin B acts on the GTP-binding protein Rho.
    Just I, Fritz G, Aktories K, Giry M, Popoff MR, Boquet P, Hegenbarth S, von Eichel-Streiber C.
    J Biol Chem; 1994 Apr 08; 269(14):10706-12. PubMed ID: 8144660
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  • 16. Rho is a negative regulator of human monocyte spreading.
    Aepfelbacher M, Essler M, Huber E, Czech A, Weber PC.
    J Immunol; 1996 Dec 01; 157(11):5070-5. PubMed ID: 8943416
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  • 17. Sphingosine 1-phosphate stimulates G(i)- and Rho-mediated vascular endothelial cell spreading and migration.
    Okamoto H, Yatomi Y, Ohmori T, Satoh K, Matsumoto Y, Ozaki Y.
    Thromb Res; 2000 Aug 01; 99(3):259-65. PubMed ID: 10942792
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  • 18. The mammalian G protein rhoC is ADP-ribosylated by Clostridium botulinum exoenzyme C3 and affects actin microfilaments in Vero cells.
    Chardin P, Boquet P, Madaule P, Popoff MR, Rubin EJ, Gill DM.
    EMBO J; 1989 Apr 01; 8(4):1087-92. PubMed ID: 2501082
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  • 19. Rho protein inactivation induced apoptosis of cultured human endothelial cells.
    Hippenstiel S, Schmeck B, N'Guessan PD, Seybold J, Krüll M, Preissner K, Eichel-Streiber CV, Suttorp N.
    Am J Physiol Lung Cell Mol Physiol; 2002 Oct 01; 283(4):L830-8. PubMed ID: 12225960
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  • 20. 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.
    Giry M, Popoff MR, von Eichel-Streiber C, Boquet P.
    Infect Immun; 1995 Oct 01; 63(10):4063-71. PubMed ID: 7558320
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