• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell Division >Caffeine as a tool for investigating the integration of Cdc25 phosphorylation, activity and ubiquitin-dependent degradation in Schizosaccharomyces pombe
【24h】

Caffeine as a tool for investigating the integration of Cdc25 phosphorylation, activity and ubiquitin-dependent degradation in Schizosaccharomyces pombe

机译：咖啡因作为研究CDC25磷酸化，活性和泛素依赖性降解在Schizosaccharomyces Pombe中的替代工具的工具

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The evolutionarily conserved Cdc25 phosphatase is an essential protein that removes inhibitory phosphorylation moieties on the mitotic regulator Cdc2. Together with the Wee1 kinase, a negative regulator of Cdc2 activity, Cdc25 is thus a central regulator of cell cycle progression in Schizosaccharomyces pombe. The expression and activity of Cdc25 is dependent on the activity of the Target of Rapamycin Complex 1 (TORC1). TORC1 inhibition leads to the activation of Cdc25 and repression of Wee1, leading to advanced entry into mitosis. Withdrawal of nitrogen leads to rapid Cdc25 degradation via the ubiquitin- dependent degradation pathway by the Pub1 E3- ligase. Caffeine is believed to mediate the override of DNA damage checkpoint signalling, by inhibiting the activity of the ataxia telangiectasia mutated (ATM)/Rad3 homologues. This model remains controversial, as TORC1 appears to be the preferred target of caffeine in vivo. Recent studies suggest that caffeine induces DNA damage checkpoint override by inducing the nuclear accumulation of Cdc25 in S. pombe. Caffeine may thus modulate Cdc25 activity and stability via inhibition of TORC1. A clearer understanding of the mechanisms by which caffeine stabilises Cdc25, may provide novel insights into how TORC1 and DNA damage signalling is integrated.
机译：进化保守的CDC25磷酸酶是一种必需蛋白质，其去除有丝分裂调节剂CDC2上的抑制磷酸化部分。因此，CDC25的CDC2活性的负调节剂与WEE1激酶一起，因此是Schizosaccharomyces Pombe中的细胞周期进展的中央调节因子。 CDC25的表达和活性取决于雷帕霉素络合物1（Torc1）的靶的活性。 Torc1抑制导致CDC25的激活和WEE1的抑制，导致进入有丝分裂。通过PUB1 E3-CIGA酶取出氮导致氮气依赖性降解途径的快速降解。通过抑制Ataxia Telanciectasia突变（ATM）/ RAD3同源物的活动，据信咖啡因介于DNA损伤检查点信号传导的覆盖。该模型仍然存在争议，因为Torc1似乎是体内咖啡因的优选靶标。最近的研究表明，咖啡因诱导DNA损伤检查点通过诱导S.Pombe中CDC25的核积累而覆盖。因此，咖啡因可以通过抑制TORC1调节CDC25活性和稳定性。更清楚地了解咖啡因稳定CDC25的机制，可以为TORC1和DNA损伤信号传导如何提供新的见解。

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