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本文引用的文献

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Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons.野生型和突变型早老素2在人胚肾293细胞和小鼠神经元中引发p53依赖性凋亡并下调早老素1的表达。
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Aurora-A overexpression reveals tetraploidization as a major route to centrosome amplification in p53-/- cells.极光激酶A的过表达揭示了四倍体化是p53基因敲除细胞中中心体扩增的主要途径。
EMBO J. 2002 Feb 15;21(4):483-92. doi: 10.1093/emboj/21.4.483.
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Difference in the centrosome duplication regulatory activity among p53 'hot spot' mutants: potential role of Ser 315 phosphorylation-dependent centrosome binding of p53.p53“热点”突变体之间中心体复制调控活性的差异：p53的Ser 315磷酸化依赖性中心体结合的潜在作用。
Oncogene. 2001 Oct 18;20(47):6851-63. doi: 10.1038/sj.onc.1204848.
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Functional analysis and intracellular localization of p53 modified by SUMO-1.SUMO-1修饰的p53的功能分析及细胞内定位
Oncogene. 2001 May 3;20(20):2587-99. doi: 10.1038/sj.onc.1204362.
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p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle.有丝分裂纺锤体短暂抑制后，p53从中心体移位及p53介导的G1期阻滞
J Biol Chem. 2001 Jun 1;276(22):19205-13. doi: 10.1074/jbc.M009528200. Epub 2001 Feb 28.
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Nucleophosmin/B23 is a target of CDK2/cyclin E in centrosome duplication.核仁磷酸蛋白/B23是中心体复制过程中CDK2/细胞周期蛋白E的一个靶点。
Cell. 2000 Sep 29;103(1):127-40. doi: 10.1016/s0092-8674(00)00093-3.
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A transactivation-deficient mouse model provides insights into Trp53 regulation and function.一种转录激活缺陷型小鼠模型为深入了解Trp53的调控和功能提供了线索。
Nat Genet. 2000 Sep;26(1):37-43. doi: 10.1038/79152.
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c-abl is involved in the association of p53 and trk A.c-abl参与p53与trk A的关联。
Oncogene. 2000 Jun 15;19(26):3032-40. doi: 10.1038/sj.onc.1203619.
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Antagonism between members of the CNC-bZIP family and the immediate-early protein IE2 of human cytomegalovirus.CNC-bZIP家族成员与人类巨细胞病毒即刻早期蛋白IE2之间的拮抗作用。
J Biol Chem. 2000 Apr 21;275(16):12313-20. doi: 10.1074/jbc.275.16.12313.
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p53 localizes to the centrosomes and spindles of mitotic cells in the embryonic chick epiblast, human cell lines, and a human primary culture: An immunofluorescence study.p53定位于胚胎鸡外胚层、人类细胞系和人类原代培养物中处于有丝分裂期细胞的中心体和纺锤体：一项免疫荧光研究。
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抑制STK15致癌活性需要一种不依赖于反式激活的p53功能。

Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function.

作者信息

Chen Shih-Shun, Chang Pi-Chu, Cheng Yu-Wen, Tang Fen-Mei, Lin Young-Sun

机构信息

Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan.

出版信息

EMBO J. 2002 Sep 2;21(17):4491-9. doi: 10.1093/emboj/cdf409.

DOI:10.1093/emboj/cdf409
PMID:12198151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC126178/
Abstract

Using a transactivation-defective p53 derivative as bait, STK15, a centrosome-associated oncogenic serine/threonine kinase, was isolated as a p53 partner. The p53-STK15 interaction was confirmed further by co-immunoprecipitation and GST pull-down studies. In co-transfection experiments, p53 suppressed STK15-induced centrosome amplification and cellular transformation in a transactivation-independent manner. The suppression of STK15 oncogenic activity by p53 might be explained in part by the finding that p53 inhibited STK15 kinase activity via direct interaction with the latter's Aurora box. Taken together, these findings revealed a novel mechanism for the tumor suppressor function of p53.

摘要

利用一种转录激活缺陷型p53衍生物作为诱饵，分离出一种与中心体相关的致癌性丝氨酸/苏氨酸激酶STK15作为p53的结合蛋白。通过免疫共沉淀和GST沉降实验进一步证实了p53与STK15的相互作用。在共转染实验中，p53以不依赖转录激活的方式抑制STK15诱导的中心体扩增和细胞转化。p53对STK15致癌活性的抑制作用，部分原因可能是p53通过与STK15的Aurora框直接相互作用抑制了其激酶活性。综上所述，这些发现揭示了p53肿瘤抑制功能的一种新机制。