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. 2010 Oct 12;285(51):39935–39942. doi: 10.1074/jbc.M110.166462

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© 2010 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 5. — Plk3 phosphorylation promotes PTEN stabilization, thereby negatively regulating the PI3K/PDK1/Akt1 signaling axis. A, paired wild-type (W) and PLK3^−/− (H) MEFs were treated with the hypoxia mimetic NiCl₂ for various times. Equal amounts of cell lysates were blotted for phospho-PTEN^{Thr-366/Ser-370}, total PTEN, phospho-GSK3β^Ser-9, total GSK3β, phospho-Akt1^Ser-437, total Akt1, and β-actin. B, paired wild-type (W) and PLK3^−/− (H) MEFs were treated with NiCl₂ for various times. Equal amounts of cell lysates were blotted for phospho-PDK1, total PDK1, and β-actin. C, paired wild-type (W) and PLK3^−/− (H) MEFs were treated with or without LiCl for 4 h after which cells were collected for lysate preparation. Equal amounts of cell lysates were blotted with antibodies to phosphorylated PTEN (p-PTEN^{Thr-366/Ser-370}), total PTEN, and β-actin. The levels of PTEN from each treatment are shown after quantification.