Regulation of mitotic progression by the spindle assembly checkpoint.

Regulation of mitotic progression by the spindle assembly checkpoint.
复制标题

DOI:
10.4161/23723548.2014.970484
复制
发表时间:
2015-01
影响因子:
2.1
通讯作者:
Nilsson J
Nilsson J
中科院分区:
其他
文献类型:
--
作者:
Lischetti T;Nilsson J

文献摘要

被引文献

相似文献

有丝分裂过程中姐妹染色单体的平等分离需要成对着丝粒与有丝分裂纺锤体相对极发出的微管建立适当的附着。纺锤体组装检查点(SAC)通过延迟姐妹分离来防止分离错误,以响应不正确的动粒-微管相互作用,并且某些检查点蛋白有助于建立适当的附着。检查点通过组装有丝分裂检查点复合物 (MCC) 来抑制后期进入,该复合物由与 Cdc20 结合的 2 个检查点蛋白 Mad2 和 BubR1 组成。外着丝粒通过检查点蛋白的募集和正确定位来充当 MCC 生产的催化剂,最近在了解如何实现这一点方面取得了显着进展。在这里,我们重点介绍了我们对动粒-检查点蛋白相互作用和 MCC 对后期促进复合物的抑制的最新进展。
Equal segregation of sister chromatids during mitosis requires that pairs of kinetochores establish proper attachment to microtubules emanating from opposite poles of the mitotic spindle. The spindle assembly checkpoint (SAC) protects against errors in segregation by delaying sister separation in response to improper kinetochore–microtubule interactions, and certain checkpoint proteins help to establish proper attachments. Anaphase entry is inhibited by the checkpoint through assembly of the mitotic checkpoint complex (MCC) composed of the 2 checkpoint proteins, Mad2 and BubR1, bound to Cdc20. The outer kinetochore acts as a catalyst for MCC production through the recruitment and proper positioning of checkpoint proteins and recently there has been remarkable progress in understanding how this is achieved. Here, we highlight recent advances in our understanding of kinetochore–checkpoint protein interactions and inhibition of the anaphase promoting complex by the MCC.