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Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death
β-catenin is constantly degraded through the ubiquitin-proteasomal pathway. We here report that a different type of β-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused β-catenin degradation in the epidermal cells through a caspase...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131442/ https://www.ncbi.nlm.nih.gov/pubmed/21383695 http://dx.doi.org/10.1038/onc.2011.49 |
Sumario: | β-catenin is constantly degraded through the ubiquitin-proteasomal pathway. We here report that a different type of β-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused β-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 β-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and β-catenin degradation induces epidermal cell death. |
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