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本文引用的文献

1
Plk1-mediated phosphorylation of Topors regulates p53 stability.Plk1介导的Topors磷酸化调节p53稳定性。
J Biol Chem. 2009 Jul 10;284(28):18588-92. doi: 10.1074/jbc.C109.001560. Epub 2009 May 27.
2
Polo-like kinases: conservation and divergence in their functions and regulation.Polo样激酶:其功能与调控的保守性与差异性
Nat Rev Mol Cell Biol. 2009 Apr;10(4):265-75. doi: 10.1038/nrm2653.
3
Ubiquitination by TOPORS regulates the prostate tumor suppressor NKX3.1.TOPORS介导的泛素化作用调控前列腺肿瘤抑制因子NKX3.1。
J Biol Chem. 2008 Feb 22;283(8):4834-40. doi: 10.1074/jbc.M708630200. Epub 2007 Dec 12.
4
The E3 ligase Topors induces the accumulation of polysumoylated forms of DNA topoisomerase I in vitro and in vivo.E3 泛素连接酶 Topors 在体外和体内均可诱导 DNA 拓扑异构酶 I 的多聚SUMO化形式积累。
FEBS Lett. 2007 Nov 27;581(28):5418-24. doi: 10.1016/j.febslet.2007.10.040. Epub 2007 Oct 30.
5
Tension-sensitive Plk1 phosphorylation on BubR1 regulates the stability of kinetochore microtubule interactions.对BubR1的张力敏感型Plk1磷酸化调节动粒微管相互作用的稳定性。
Genes Dev. 2007 Sep 1;21(17):2205-19. doi: 10.1101/gad.436007.
6
Polo-like kinase controls vertebrate spindle elongation and cytokinesis.Polo-like 激酶控制脊椎动物纺锤体的伸长和胞质分裂。
PLoS One. 2007 May 2;2(5):e409. doi: 10.1371/journal.pone.0000409.
7
Microtubule disruptors and their interaction with biotransformation enzymes.微管破坏剂及其与生物转化酶的相互作用。
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005 Dec;149(2):213-5.
8
Normal cells, but not cancer cells, survive severe Plk1 depletion.正常细胞而非癌细胞在严重的Plk1缺失情况下仍能存活。
Mol Cell Biol. 2006 Mar;26(6):2093-108. doi: 10.1128/MCB.26.6.2093-2108.2006.
9
Topors acts as a SUMO-1 E3 ligase for p53 in vitro and in vivo.在体内和体外,Topors作为p53的一种SUMO-1 E3连接酶发挥作用。
FEBS Lett. 2005 Sep 12;579(22):5007-12. doi: 10.1016/j.febslet.2005.07.088.
10
topors, a p53 and topoisomerase I-binding RING finger protein, is a coactivator of p53 in growth suppression induced by DNA damage.TOPORS是一种与p53及拓扑异构酶I结合的环状结构域蛋白,在DNA损伤诱导的生长抑制过程中作为p53的共激活因子。
Oncogene. 2005 May 12;24(21):3385-96. doi: 10.1038/sj.onc.1208554.

Plk1 对 Topors 的磷酸化作用参与了其降解。

Plk1 phosphorylation of Topors is involved in its degradation.

机构信息

College of Chemistry, Sichuan University, Chengdu 610064, China.

出版信息

Mol Biol Rep. 2010 Jul;37(6):3023-8. doi: 10.1007/s11033-009-9871-1. Epub 2009 Oct 11.

DOI:10.1007/s11033-009-9871-1
PMID:19821153
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4965875/
Abstract

Topors is a DNA topoisomerase I- and p53-binding protein, and mainly functions as a p53 regulator. Accumulating evidence also supports the notion that Topors plays the role as a negative regulator of cell growth, and possibly as a tumor suppressor. Here, we demonstrated that Topors is also involved in normal mitotic progression, since Topors depletion delays mitotic entry and affects mitotic progression. Furthermore, Topors is degradated in response to the activation of the spindle checkpoint. Significantly, Polo-like kinase 1 (Plk1)-associated phosphorylation of Topors at S718 is essential for nocodazole-induced degradation of Topors.

摘要

拓扑异构酶 I 和 p53 结合蛋白 Topors 主要作为 p53 调节因子发挥作用。越来越多的证据也支持这样一种观点,即 Topors 作为细胞生长的负调节剂发挥作用,并可能作为肿瘤抑制因子发挥作用。在这里,我们证明 Topors 也参与正常有丝分裂进程,因为 Topors 耗竭延迟有丝分裂进入并影响有丝分裂进程。此外,Topors 响应纺锤体检查点的激活而降解。重要的是,Polo 样激酶 1(Plk1)相关的 Topors 的 S718 磷酸化对于诺考达唑诱导的 Topors 降解是必需的。