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Up-regulation of RhoB by Large Clostridial Cytotoxins
Contributor(s): Hülsenbeck, Johannes (Author)
ISBN: 3639001680     ISBN-13: 9783639001686
Publisher: VDM Verlag Dr. Mueller E.K.
OUR PRICE:   $50.27  
Product Type: Paperback
Published: April 2008
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BISAC Categories:
- Science | Life Sciences - Biochemistry
Physical Information: 0.14" H x 6" W x 9" (0.23 lbs) 68 pages
 
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Clostridium difficile toxins A (TcdA) and B (TcdB) are monoglucosyl-transferases that inactivate RhoA, Rac1, and Cdc42. By these means, the toxins cause actin reorganisation (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.