| First Author | Huelsenbeck J | Year | 2012 |
| Journal | FEBS Lett | Volume | 586 |
| Issue | 20 | Pages | 3665-73 |
| PubMed ID | 22982107 | Mgi Jnum | J:190123 |
| Mgi Id | MGI:5448101 | Doi | 10.1016/j.febslet.2012.08.024 |
| Citation | Huelsenbeck J, et al. (2012) Cytoprotective effect of the small GTPase RhoB expressed upon treatment of fibroblasts with the Ras-glucosylating Clostridium sordellii lethal toxin. FEBS Lett 586(20):3665-73 |
| abstractText | Mono-glucosylation of (H/K/N)Ras by Clostridium sordellii lethal toxin (TcsL) blocks critical survival signaling pathways, resulting in apoptosis. In this study, TcsL and K-Ras knock-down by siRNA are presented to result in expression of the cell death-regulating small GTPase RhoB. TcsL-induced RhoB expression is based on transcriptional activation involving p38(alpha) MAP kinase. Newly synthesized RhoB protein is rapidly degraded in a proteasome- and a caspase-dependent manner, providing first evidence for caspase-dependent degradation of a Rho family protein. Although often characterised as a pro-apoptotic protein, RhoB suppresses caspase-3 activation in TcsL-treated fibroblasts. The finding on the cytoprotective activity of RhoB in TcsL-treated cells re-enforces the concept that RhoB exhibits cytoprotective rather than pro-apoptotic activity in a cellular background of inactive Ras. |
