Evidence map›Paper›PMID 25605730›Full record

ArticleThe Journal of biological chemistry2015

Oncoprotein YAP regulates the spindle checkpoint activation in a mitotic phosphorylation-dependent manner through up-regulation of BubR1.

Shuping Yang, Lin Zhang, Xingcheng Chen, Yuanhong Chen, Jixin Dong

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 29 citations in OpenAlex.

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  13. Mechanisms of Hippo pathway regulation.Genes & development · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Shuping YangFrom the Department of Oncology, Shandong Provincial Hospital affiliated with Shandong University, Jinan, Shandong 250021, China and the Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Lin Zhangthe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Xingcheng Chenthe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Yuanhong Chenthe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198.
Jixin Dongthe Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198 dongj@unmc.edu.
University of Nebraska Medical Center · USShandong University · CN

Funding

Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
Regulation and Functional Dissection of YAP in MitosisR01GM109066 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DONG, JIXIN · 2014 to 2018
$1.4M
NIGMS NIH HHS 5P30 GM106397NIGMS NIH HHS P30 GM106397NIGMS NIH HHS R01 GM109066
6 · The paper itself

Abstract

The transcriptional co-activator YAP (Yes-associated protein) functions as an oncogene; however, it is largely unclear how YAP exerts its oncogenic role. In this study, we further explored the functional significance of YAP and its mitotic phosphorylation in the spindle checkpoint. We found that the dynamic mitotic phosphorylation of YAP was CDC14-dependent. We also showed that YAP was required for the spindle checkpoint activation induced by spindle poisons. Mitotic phosphorylation of YAP was required for activation of the spindle checkpoint. Furthermore, enhanced expression of active YAP hyperactivated the spindle checkpoint and induced mitotic defects in a mitotic phosphorylation-dependent manner. Mechanistically, we documented that mitotic phosphorylation of YAP controlled transcription of genes associated with the spindle checkpoint. YAP constitutively associated with BubR1 (BUB1-related protein kinase), and knockdown of BubR1 relieved YAP-driven hyperactivation of the spindle checkpoint. Finally, we demonstrated that YAP promoted epithelial cell invasion via both mitotic phosphorylation and BubR1-dependent mechanisms. Together, our results reveal a novel link between YAP and the spindle checkpoint and indicate a potential mechanism underlying the oncogenic function of YAP through dysregulation of the spindle checkpoint.

Indexed as

Transcription, GeneticCell Cycle ProteinsDual-Specificity PhosphatasesGene Expression RegulationHumansMCF-7 CellsM Phase Cell Cycle CheckpointsNeoplasmsNuclear ProteinsPhosphorylationProtein Serine-Threonine KinasesTranscription FactorsBUB1 protein, humanCDC14B protein, humanCell Cycle ProteinsDual-Specificity PhosphatasesNuclear ProteinsProtein Serine-Threonine KinasesTranscription FactorsYY1AP1 protein, humanBubR1Hippo PathwayMitosisOncogenePhosphorylationSpindle CheckpointYes-associated Protein (YAP)

Identifiers

PMID25605730
PMCPMC4358258
OpenAlexW2018172401

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.