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本文引用的文献

1
BubR1 N terminus acts as a soluble inhibitor of cyclin B degradation by APC/C(Cdc20) in interphase.在间期,BubR1的N端作为一种可溶性抑制剂,抑制周期蛋白B被后期促进复合体/细胞周期蛋白依赖性激酶20(APC/C(Cdc20))降解。
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2
Phosphorylation sites in BubR1 that regulate kinetochore attachment, tension, and mitotic exit.BubR1中调节动粒附着、张力和有丝分裂退出的磷酸化位点。
J Cell Biol. 2008 Nov 17;183(4):667-80. doi: 10.1083/jcb.200805163.
3
Regulation of kinetochore recruitment of two essential mitotic spindle checkpoint proteins by Mps1 phosphorylation.Mps1磷酸化对两种重要有丝分裂纺锤体检查点蛋白着丝粒募集的调控。
Mol Biol Cell. 2009 Jan;20(1):10-20. doi: 10.1091/mbc.e08-03-0324. Epub 2008 Oct 15.
4
Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery.Polo样激酶-1由极光激酶A激活,以促进检查点恢复。
Nature. 2008 Sep 4;455(7209):119-23. doi: 10.1038/nature07185. Epub 2008 Jul 9.
5
Bora and the kinase Aurora a cooperatively activate the kinase Plk1 and control mitotic entry.博拉蛋白与极光激酶A协同激活 polo 样激酶 1 并控制有丝分裂进入。
Science. 2008 Jun 20;320(5883):1655-8. doi: 10.1126/science.1157425.
6
Polo on the Rise-from Mitotic Entry to Cytokinesis with Plk1.Polo激酶的崛起——从有丝分裂进入到细胞分裂与Plk1的作用
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7
Aurora B kinase and protein phosphatase 1 have opposing roles in modulating kinetochore assembly.极光激酶B和蛋白磷酸酶1在调节动粒组装中具有相反作用。
J Cell Biol. 2008 Apr 21;181(2):241-54. doi: 10.1083/jcb.200710019.
8
Linking kinetochore-microtubule binding to the spindle checkpoint.将动粒-微管结合与纺锤体检查点相联系。
Dev Cell. 2008 Apr;14(4):474-9. doi: 10.1016/j.devcel.2008.03.015.
9
The mitotic checkpoint kinase NEK2A regulates kinetochore microtubule attachment stability.有丝分裂检查点激酶NEK2A调节动粒微管附着稳定性。
Oncogene. 2008 Jul 3;27(29):4107-14. doi: 10.1038/onc.2008.34. Epub 2008 Feb 25.
10
Mps1 phosphorylates Borealin to control Aurora B activity and chromosome alignment.Mps1使Borealin磷酸化以控制极光激酶B的活性和染色体排列。
Cell. 2008 Jan 25;132(2):233-46. doi: 10.1016/j.cell.2007.11.046.

纺锤体检查点中的激酶信号传导。

Kinase signaling in the spindle checkpoint.

作者信息

Kang Jungseog, Yu Hongtao

机构信息

Department of Pharmacology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

出版信息

J Biol Chem. 2009 Jun 5;284(23):15359-63. doi: 10.1074/jbc.R900005200. Epub 2009 Feb 19.

DOI:10.1074/jbc.R900005200
PMID:19228686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2708832/
Abstract

The spindle checkpoint is a cell cycle surveillance system that ensures the fidelity of chromosome segregation. In mitosis, it elicits the "wait anaphase" signal to inhibit the anaphase-promoting complex or cyclosome until all chromosomes achieve bipolar microtubule attachment and align at the metaphase plate. Because a single kinetochore unattached to microtubules activates the checkpoint, the wait anaphase signal is thought to be generated by this kinetochore and is then amplified and distributed throughout the cell to inhibit the anaphase-promoting complex/cyclosome. Several spindle checkpoint kinases participate in the generation and amplification of this signal. Recent studies have begun to reveal the activation mechanisms of these checkpoint kinases. Increasing evidence also indicates that the checkpoint kinases not only help to generate the wait anaphase signal but also actively correct kinetochore-microtubule attachment defects.

摘要

纺锤体检查点是一种细胞周期监测系统,可确保染色体分离的准确性。在有丝分裂过程中,它引发“等待后期”信号,以抑制后期促进复合物或细胞周期体,直到所有染色体实现双极微管附着并排列在中期板上。由于单个未附着微管的动粒会激活检查点,因此人们认为“等待后期”信号是由该动粒产生的,然后在整个细胞中放大并传播,以抑制后期促进复合物/细胞周期体。几种纺锤体检查点激酶参与了该信号的产生和放大。最近的研究开始揭示这些检查点激酶的激活机制。越来越多的证据还表明,检查点激酶不仅有助于产生“等待后期”信号,还能积极纠正动粒-微管附着缺陷。