0000000000645073

AUTHOR

Helma Tatge

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Clostridium difficile toxin A induces expression of the stress-induced early gene product RhoB.

2004

Clostridium difficile toxin A monoglucosylates the Rho family GTPases Rho, Rac, and Cdc42. Glucosylation leads to the functional inactivation of Rho GTPases and causes disruption of the actin cytoskeleton. A cDNA microarray revealed the immediate early gene rhoB as the gene that was predominantly up-regulated in colonic CaCo-2 cells after treatment with toxin A. This toxin A effect was also detectable in epithelial cells such as HT29 and Madin-Darby canine kidney cells, as well as NIH 3T3 fibroblasts. The expression of RhoB was time-dependent and correlated with the morphological changes of cells. The up-regulation of RhoB was approximately 15-fold and was based on the de novo synthesis of …

RHOAPyridinesRHOBBacterial ToxinsClostridium difficile toxin ARAC1GTPaseBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicGene productEnterotoxinsStress PhysiologicalRhoB GTP-Binding ProteinHumansrhoB GTP-Binding ProteinMolecular BiologyOligonucleotide Array Sequence AnalysisbiologyImidazolesCell BiologyRhoBClostridium difficileActin cytoskeletonMolecular biologyUp-Regulationbiology.proteinGene expressionCaco-2 CellsThe Journal of biological chemistry
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