Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition

Kazuhiro Katayama; Naoya Fujita; Takashi Tsuruo

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Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition

机译：Akt /蛋白激酶B依赖的磷酸化和WEE1Hu的失活促进了G2 / M过渡的细胞周期进程

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The serine/threonine kinase Akt is known to promote cell growth by regulating the cell cycle in G₁ phase through activation of cyclin/Cdk kinases and inactivation of Cdk inhibitors. However, how the G₂/M phase is regulated by Akt remains unclear. Here, we show that Akt counteracts the function of WEE1Hu. Inactivation of Akt by chemotherapeutic drugs or the phosphatidylinositide-3-OH kinase inhibitor LY294002 induced G₂/M arrest together with the inhibitory phosphorylation of Cdc2. Because the increased Cdc2 phosphorylation was completely suppressed by wee1hu gene silencing, WEE1Hu was associated with G₂/M arrest induced by Akt inactivation. Further analyses revealed that Akt directly bound to and phosphorylated WEE1Hu during the S to G₂ phase. Serine-642 was identified as an Akt-dependent phosphorylation site. WEE1Hu kinase activity was not affected by serine-642 phosphorylation. We revealed that serine-642 phosphorylation promoted cytoplasmic localization of WEE1Hu. The nuclear-to-cytoplasmic translocation was mediated by phosphorylation-dependent WEE1Hu binding to 14-3-3θ but not 14-3-3β or -σ. These results indicate that Akt promotes G₂/M cell cycle progression by inducing phosphorylation-dependent 14-3-3θ binding and cytoplasmic localization of WEE1Hu.

机译：已知丝氨酸/苏氨酸激酶Akt通过激活cyclin / Cdk激酶和使Cdk抑制剂失活，通过调节G _{1 期的细胞周期来促进细胞生长。但是，如何通过Akt调节G _{2 / M相仍然不清楚。在这里，我们显示Akt抵消了WEE1Hu的功能。化疗药物或磷脂酰肌醇-3-OH激酶抑制剂LY294002使Akt失活会导致G _{2 / M阻滞，同时抑制Cdc2。由于 wee1hu 基因沉默完全抑制了Cdc2磷酸化的增加，因此WEE1Hu与Akt失活诱导的G _{2 / M阻滞有关。进一步的分析表明，Akt在S到G _{2 阶段直接结合并磷酸化WEE1Hu。丝氨酸642被确定为Akt依赖的磷酸化位点。 WEE1Hu激酶活性不受丝氨酸642磷酸化的影响。我们发现丝氨酸642磷酸化促进WEE1Hu的细胞质定位。核到细胞质的易位是通过磷酸化依赖性的WEE1Hu结合14-3-3θ而不是14-3-3β或-σ来介导的。这些结果表明，Akt通过诱导WEE1Hu的磷酸化依赖性14-3-3θ结合和细胞质定位来促进G _{2 / M细胞周期进程。}}}}}} 展开▼

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《Molecular and Cellular Biology》 |2005年第13期|共13页

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Kazuhiro Katayama; Naoya Fujita; Takashi Tsuruo;
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中图分类细胞生物学;

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2. Arterialization of a vein graft promotes cell cycle progression through Akt and p38 mitogen-activated protein kinase pathways: impact of the preparation procedure. [J] . Chung AW, Wong J, Luo H, The Canadian journal of cardiology . 2007,第14期

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3. MAP kinase inactivation is required only for G2-M phase transition in early embryogenesis cell cycles of the starfishes Marthasterias glacialis and Astropecten aranciacus [J] . Fisher D., Simon MN., Keyse S., Developmental biology . 1998,第1期

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6. Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition [O] . Kazuhiro Katayama, Naoya Fujita, Takashi Tsuruo 2005

机译：Akt /蛋白激酶B依赖的磷酸化和WEE1Hu的失活促进了G2 / M过渡的细胞周期进程

7. Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition [O] . Katayama, Kazuhiro, Fujita, Naoya, Tsuruo, Takashi 2005

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Akt/Protein Kinase B-Dependent Phosphorylation and Inactivation of WEE1Hu Promote Cell Cycle Progression at G2/M Transition

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