...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The Saccharomyces cerevisiae 14-3-3 proteins Bmh1 and Bmh2 directly influence the DNA damage-dependent functions of Rad53
【24h】

The Saccharomyces cerevisiae 14-3-3 proteins Bmh1 and Bmh2 directly influence the DNA damage-dependent functions of Rad53

机译：酿酒酵母14-3-3蛋白Bmh1和Bmh2直接影响Rad53的DNA损伤依赖性功能

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In this study, we mutated autophosphorylation sites in Rad53 based on their conservation with previously identified autophosphorylation sites in the mammalian Rad53 ortholog, Chk2. As with wild-type Rad53, the autophosphorylation mutant, rad53-TA, undergoes Mec1 /Tel1-dependent interactions with Rad9 and Dun1 in response to genotoxic stress. Whereas rad53-TA in vitro kinase activity is severely impaired, the rad53-TA strains are not completely deficient for cell-cycle checkpoint functions, indicating that the mutant kinase retains a basal level of function. We describe a genetic interaction among Rad53, Dun1, and the 14-3-3 proteins Bmh1 and Bmh2 and present evidence that 14-3-3 proteins directly facilitate Rad53 function in vivo. The data presented account for the previously observed checkpoint defects associated with 14-3-3 mutants in Saccharomyces pombe and Saccharomyces cerevisiae. The 14-3-3 functional interaction appears to modulate Rad53 activity, reminiscent of 14-3-3′s effect on human Raf1 kinase and distinct from the indirect mode of regulation by 14-3-3 observed for Chk1 or Cdc25.
机译：在这项研究中，我们基于与哺乳动物Rad53直系同源物Chk2中先前确定的自磷酸化位点的保守性，将Rad53中的自磷酸化位点突变。与野生型Rad53一样，自磷酸化突变体rad53-TA响应基因毒性胁迫而与Rad9和Dun1进行Mec1 / Tel1依赖性相互作用。 rad53-TA体外激酶活性严重受损，而rad53-TA菌株并非完全缺乏细胞周期检查点功能，这表明突变型激酶保留了基本的功能水平。我们描述了Rad53，Dun1和14-3-3蛋白Bmh1和Bmh2之间的遗传相互作用，并提供证据表明14-3-3蛋白直接促进Rad53在体内的功能。所提供的数据解释了以前观察到的与粟酒酵母和酿酒酵母中14-3-3突变体相关的检查点缺陷。 14-3-3的功能相互作用似乎可以调节Rad53的活性，让人联想到14-3-3对人Raf1激酶的作用，并且与14-13对Chk1或Cdc25的间接调节模式不同。

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