| First Author | Omori E | Year | 2011 |
| Journal | Oncogene | Volume | 30 |
| Issue | 30 | Pages | 3336-44 |
| PubMed ID | 21383695 | Mgi Jnum | J:174637 |
| Mgi Id | MGI:5140268 | Doi | 10.1038/onc.2011.49 |
| Citation | Omori E, et al. (2011) Non-canonical beta-catenin degradation mediates reactive oxygen species-induced epidermal cell death. Oncogene 30(30):3336-44 |
| abstractText | beta-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we report that a different type of beta-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused beta-catenin degradation in the epidermal cells through a caspase-dependent mechanism, which results in disruption of cell adhesion. Disruption of cell adhesion increased ROS and activated caspases. Upregulation of the intact beta-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and beta-catenin degradation induces epidermal cell death. |
