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Non-canonical ?-catenin degradation mediates reactive oxygen species-induced epidermal cell death.


ABSTRACT: ?-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we report that a different type of ?-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused ?-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 ?-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and ?-catenin degradation induces epidermal cell death.

SUBMITTER: Omori E 

PROVIDER: S-EPMC3131442 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature

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Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death.

Omori E E   Matsumoto K K   Ninomiya-Tsuji J J  

Oncogene 20110307 30


β-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we 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 accumul  ...[more]

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