Non-canonical [beta]-catenin degradation mediates reactive oxygen species-induced epidermal cell death
b-Catenin is constantly degraded through the ubiquitinproteasomal pathway. In this study, we report that a different type of b-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused b-catenin degradation in the epidermal cells through...
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Veröffentlicht in: | Oncogene 2011-07, Vol.30 (30), p.3336 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | b-Catenin is constantly degraded through the ubiquitinproteasomal pathway. In this study, we report that a different type of b-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused b-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 b-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and b-catenin degradation induces epidermal cell death. [PUBLICATION ABSTRACT] |
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ISSN: | 0950-9232 1476-5594 |
DOI: | 10.1038/onc.2011.49 |