首页> 外文期刊>Stem Cells >p55Cdc/cdc20 overexpression promotes early g1/s transition in myeloid cells.
【24h】

p55Cdc/cdc20 overexpression promotes early g1/s transition in myeloid cells.

机译:p55Cdc / cdc20过表达促进骨髓细胞中早期的g1 / s过渡。

获取原文
获取原文并翻译 | 示例
           

摘要

p55Cdc/Cdc20 is expressed in cycling mammalian cells and has been shown to be an activator of the mitotic spindle assembly checkpoint. We previously showed that overexpression of p55Cdc/Cdc20 in myeloid cells resulted in accelerated apoptosis and inhibition of granulocyte differentiation in the murine myeloid cell line 32Dcl3. p55Cdc/Cdc20 protein expression is detected in cells at late G1 phase of the cell cycle but is maximal during G2 phase. We report in this paper that inducible expression of p55Cdc/Cdc20 in 32Dcl3 cells results in premature transition from G1 to S phase. To characterize the mechanism of this early transition, we examined the expression of critical regulatory proteins during the cell cycle. Although expression of cyclin D, cyclin E, cdk2, and cdc2 did not change significantly between p55Cdc/Cdc20-overexpressing and control cells, p27Kip1 protein levels were lower and cdk2 activity higher during G1 to S transition in p55Cdc/Cdc20-overexpressing cells compared to control cells. Cyclin B1 levels were lower at early G1 phase in cells overexpressing p55Cdc/Cdc20. Our results suggest that p55Cdc/Cdc20 may play an important role in G1 to S transition during myelopoiesis.
机译:p55Cdc / Cdc20在循环的哺乳动物细胞中表达,并已证明是有丝分裂纺锤体装配检查点的激活剂。我们以前显示髓细胞中p55Cdc / Cdc20的过表达导致鼠髓细胞系32Dcl3的凋亡加速和粒细胞分化的抑制。在细胞周期的G1晚期,在细胞中检测到p55Cdc / Cdc20蛋白表达,但在G2阶段最大。我们在本文中报道,p55Cdc / Cdc20在32Dcl3细胞中的诱导表达导致从G1到S期的过早转变。为了表征这种早期过渡的机制,我们检查了细胞周期中关键调节蛋白的表达。尽管在p55Cdc / Cdc20过表达和对照细胞之间,细胞周期蛋白D,细胞周期蛋白E,cdk2和cdc2的表达没有显着变化,但与p55Cdc / Cdc20过表达的细胞相比,p27Kip1蛋白水平较低,而cdk2活性较高。控制细胞。在过表达p55Cdc / Cdc20的细胞中,早期G1期细胞周期蛋白B1水平较低。我们的结果表明,p55Cdc / Cdc20在骨髓生成过程中可能在G1向S的转变中起重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号