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
Hauptverfasser: Omori, E, Matsumoto, K, Ninomiya-tsuji, J
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Ninomiya-tsuji, J
description 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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subjects Apoptosis
Cell adhesion & migration
Cell death
Enzymes
Oncology
title Non-canonical [beta]-catenin degradation mediates reactive oxygen species-induced epidermal cell death
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