...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biochemical and Biophysical Research Communications >Involvement of a centrosomal protein kendrin in the maintenance of centrosome cohesion by modulating Nek2A kinase activity.
【24h】

Involvement of a centrosomal protein kendrin in the maintenance of centrosome cohesion by modulating Nek2A kinase activity.

机译：通过调节Nek2A激酶活性，中心体蛋白kendrin参与维持中心体凝聚力。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

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

摘要

Centrosome cycle is strictly coordinated with chromosome duplication cycle to ensure the faithful segregation of chromosomes. Centrosome duplication occurs from the beginning of S phase, and the duplicated centrosomes are held together by centrosome cohesion to function as a single microtubule organizing center during interphase. At late G2 phase centrosome cohesion is disassembled by Nek2A kinase-mediated phosphorylation and, as a consequence, centrosomes are split and constitute spindle poles in mitosis. It has been reported that depletion of a centrosomal protein kendrin (also named pericentrin) induces premature centrosome splitting in interphase, however, it remains unknown how kendrin contributes to the maintenance of centrosome cohesion. Here we show that kendrin associates with Nek2A kinase, which exhibits considerably low activity. Nek2A kinase activity is inhibited in vitro by addition of the Nek2A-binding region of kendrin in a dose-dependent manner. Furthermore, ectopic expression of the same region decreases the number of the cells with split centrosomes at late G2 phase. Taken together, these results suggest that kendrin anchors Nek2A and suppresses its kinase activity at the centrosomes, and thus, is involved in the mechanism to prevent premature centrosome splitting during interphase.
机译：中心体周期与染色体复制周期严格协调，以确保染色体的忠实分离。从S期开始发生质体复制，并且复制的质体通过质体凝聚力保持在一起，从而在相间充当单个微管组织中心。在G2期晚期，Nek2A激酶介导的磷酸化使中心体凝聚力解体，结果，中心体分裂并在有丝分裂中构成纺锤体极。据报道，中心体蛋白kendrin（也称为pericentrin）的消耗会引起相间过早的中心体分裂，但是，尚不清楚kendrin如何促进中心体凝聚力的维持。在这里，我们显示肯德林与Nek2A激酶缔合，后者表现出相当低的活性。 Nek2A激酶活性在体外通过以剂量依赖性方式添加肯德林的Nek2A结合区而受到抑制。此外，同一区域的异位表达减少了G2期晚期分裂中心体的细胞数量。综上所述，这些结果表明，kendrin锚定Nek2A并抑制其在中心体的激酶活性，因此参与了预防相间过早中心体分裂的机制。

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