Up-regulation of RhoB by Large Clostridial Cytotoxins - Hülsenbeck, Johannes
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Clostridium difficile toxins A (TcdA) and B (TcdB) are mono-glucosyltransferases that inactivate RhoA, Rac1, and Cdc42. By these means, the toxins cause actin re-organisation (cytopathic effect) and apoptosis (cytotoxic effect). The cytotoxic effect has generally been attributed to the inactivation of RhoA. Treatment of cultured cells with Clostridium difficile toxin A (TcdA) also causes RhoB up-regulation. This study focuses on the up-regulation of RhoB and its functional consequences in toxin-treated cells.RhoB is up-regulated after treatment of fibroblasts with RhoA/B/C (TcdB, C. limosum…mehr

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Produktbeschreibung
Clostridium difficile toxins A (TcdA) and B (TcdB) are mono-glucosyltransferases that inactivate RhoA, Rac1, and Cdc42. By these means, the toxins cause actin re-organisation (cytopathic effect) and apoptosis (cytotoxic effect). The cytotoxic effect has generally been attributed to the inactivation of RhoA. Treatment of cultured cells with Clostridium difficile toxin A (TcdA) also causes RhoB up-regulation. This study focuses on the up-regulation of RhoB and its functional consequences in toxin-treated cells.RhoB is up-regulated after treatment of fibroblasts with RhoA/B/C (TcdB, C. limosum C3) or H/K/N-Ras (C. sordellii lethal toxin) inactivating toxins. The up-regulation is based on transcriptional activation. p38 MAP kinase is identified as enhancer of RhoB up-regulation. Finally, RhoB is found to regulate TcdB-induced apoptosis.
Autorenporträt
Hülsenbeck, Johannes§Johannes Hülsenbeck (_6.3.1978) studied biochemistry at the Ruhr-Universität Bochum and the Gottfried Wilhelm Leibniz Universität Hannover. He worked on his thesis in the Institute of Toxicology at the Medizinische Hochschule Hannover until 2007. Since then, he works at the Institute of Toxicology at the Johannes Gutenberg Universität Mainz.