Evidence map›Paper›PMID 28780319›Full record

ArticleCellular signalling2017

CDK1-mediated mitotic phosphorylation of PBK is involved in cytokinesis and inhibits its oncogenic activity.

Seth Stauffer, Yongji Zeng, Jiuli Zhou, Xingcheng Chen, Yuanhong Chen, Jixin Dong

Abstract read
In one paragraph

Article in Cellular signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Biochemistry and biophysics reports · 2023
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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

6 authors at 1 institution in 1 country.

Seth StaufferEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Yongji ZengEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Jiuli ZhouEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Xingcheng ChenEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Yuanhong ChenEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States.
Jixin DongEppley Institute for Research in Cancer, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, United States; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, United States. Electronic address: dongj@unmc.edu.
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
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
NCI NIH HHS P30 CA036727NIGMS NIH HHS P30 GM106397NIGMS NIH HHS R01 GM109066
6 · The paper itself

Abstract

PDZ-binding kinase (PBK) plays a major role in proliferation and in safeguarding mitotic fidelity in cancer cells. Frequently upregulated in many cancers, PBK drives tumorigenesis and metastasis. PBK has been shown to be phosphorylated in mitosis by cyclin-dependent kinase 1 (CDK1)/cyclin B, however, no studies have been done examining PBK mitotic phosphorylation in oncogenesis. Additionally to the previously identified Threonine-9 phosphorylation, we found that Threonine-24, Serine-32, and Serine-59 of PBK are also phosphorylated. PBK is phosphorylated in vitro and in cells by CDK1 during antimitotic drug-induced mitotic arrest and in normal mitosis. We demonstrated that mitotic phosphorylation of Threonine-9 is involved in cytokinesis. The non-phosphorylatable mutant PBK-T9A augments tumorigenesis to a greater extent than wild type PBK in breast cancer cells, suggesting that PBK mitotic phosphorylation inhibits its tumor promoting activity. The PBK-T9A mutant also transforms and increases the proliferation of immortalized breast epithelial cells. Collectively, this study reveals that CDK1-mediated mitotic phosphorylation of PBK is involved in cytokinesis and inhibits its oncogenic activity.

Indexed as

CytokinesisMitosisCarcinogenesisCDC2 Protein KinaseCell Line, TumorCell ProliferationHEK293 CellsHeLa CellsHumansMitogen-Activated Protein Kinase KinasesMutationPhosphorylationSerineThreonineCDC2 Protein KinaseCDK1 protein, humanMitogen-Activated Protein Kinase KinasesPDZ-binding kinaseSerineThreonineCDK1CytokinesisMitotic phosphorylationOncogenesisPBK

Identifiers

PMID28780319
PMCPMC5592141
OpenAlexW2744541013

What OpenQuestion holds

Textmetadata
LicenceTDM
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.