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JCS ePress online publication date 31 Jul 2007
doi: 10.1242/jcs.03473

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Research Article

GSK-3{beta} acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 in ceramide-induced mitochondrial apoptosis


Chiou-Feng Lin, Chia-Ling Chen, Chi-Wu Chiang, Ming-Shiou Jan, Wei-Ching Huang, and Yee-Shin Lin*
* Author for correspondence (e-mail: yslin1{at}mail.ncku.edu.tw)

The signaling of glycogen synthase kinase-3{beta} (GSK-3{beta}) has been implicated in stress-induced apoptosis. However, the pro-apoptotic role of GSK-3{beta} is still unclear. Here, we show the involvement of GSK-3{beta} in ceramide-induced mitochondrial apoptosis. Ceramide induced GSK-3{beta} activation via protein dephosphorylation at serine 9. We previously reported that ceramide induced caspase-2 and caspase-8 activation, Bid cleavage, mitochondrial damage, and apoptosis. In this study, we found that caspase-2 activation and the subsequent apoptotic events were abolished by the GSK-3{beta} inhibitors lithium chloride and SB216763, and by GSK-3{beta} knockdown using short interfering RNA. We also found that ceramide-activated protein phosphatase 2A (PP2A) indirectly caused GSK-3{beta} activation, and that the PP2A-regulated PI 3-kinase-Akt pathway was involved in GSK-3{beta} activation. These results indicate a role for GSK-3{beta} in ceramide-induced apoptosis, in which GSK-3{beta} acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.


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© The Company of Biologists Ltd 2007