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

被引：10

作者：

Omori, E. ^{[1
]}

Matsumoto, K. ^{[2
]}

Ninomiya-Tsuji, J. ^{[1
]}

机构：

[1] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA

[2] Nagoya Univ, Grad Sch Sci, Dept Mol Biol, Nagoya, Aichi 4648601, Japan

来源：

ONCOGENE | 2011年 / 30卷 / 30期

基金：

美国国家卫生研究院;

关键词：

apoptosis; beta-catenin; caspase; epidermis; reactive oxygen species; TUMOR-NECROSIS-FACTOR; IL-1 SIGNALING PATHWAY; PROTEOLYTIC CLEAVAGE; FACTOR-ALPHA; KINASE TAK1; HELA-CELLS; TNF-ALPHA; KAPPA-B; ACTIVATION; APOPTOSIS;

D O I：

10.1038/onc.2011.49

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. Oncogene (2011) 30, 3336-3344; doi:10.1038/onc.2011.49; published online 7 March 2011

引用

页码：3336 / 3344

页数：9

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