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- W2317698983 abstract "Loss of functional pancreatic beta-cells is a critical event in the pathogenesis of diabetes and there is mounting evidence that chronic stress of the endoplasmic reticulum (ER) contributes significantly to beta-cell dysfunction and apoptotic death. Bax and Bak are known to control the execution of mitochondrial apoptosis and have recently been suggested to also regulate ER physiology and stress signalling. In this study we set out to determine the relative importance of Bax and Bak for beta-cell death and their putative roles in beta-cell ER stress under diabetogenic conditions. We generated lines of mice in which the single or combined knockout of Bax and/or Bak can be induced specifically in the islet beta-cells. Single and double knockout cells were subjected to staurosporine, thapsigargin, and glucolipotoxic conditions. The kinetics of beta-cell death were evaluated by continuous imaging for up to 72 hours. The activation of islet ER stress was evaluated by quantitative PCR following culture in thapsigargin or glucolipotoxic conditions over 48 hours. Our data demonstrate that the loss of Bax and Bak protects beta-cells from staurosporine-induced death, and suggest they are important for beta-cell loss under conditions of glucolipotoxicity and chronic ER stress. Interestingly, double Bax-Bak knockout resulted in an acute and transient up-regulation of the islet ER stress response. Together, these data suggest that Bax and Bak, both separately and in combination, are important for beta-cell loss in diabetes and have novel roles in the regulation of beta-cell organelle stress upstream of apoptosis execution." @default.
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- W2317698983 date "2012-10-01" @default.
- W2317698983 modified "2023-10-18" @default.
- W2317698983 title "Combined and Individual Roles of Bax and Bak in Beta-Cell Stress Signalling and Death" @default.
- W2317698983 doi "https://doi.org/10.1016/j.jcjd.2012.07.415" @default.
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