Evidence map›Paper›PMID 16784539›Full record

ArticleMolecular cancer2006

The p53-targeting human phosphatase hCdc14A interacts with the Cdk1/cyclin B complex and is differentially expressed in human cancers.

Michelle T Paulsen, Adrienne M Starks, Frederick A Derheimer, Sheela Hanasoge, Liwu Li, Jack E Dixon, Mats Ljungman

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

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  5. The Multiple Roles of the Cdc14 Phosphatase in Cell Cycle Control.International journal of molecular sciences · 2020
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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

7 authors at 3 institutions in 1 country.

Michelle T PaulsenDepartment of Radiation Oncology, Division of Radiation & Cancer Biology, University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA. tenbroek@umich.edu
Adrienne M Starks
Frederick A Derheimer
Sheela Hanasoge
Liwu Li
Jack E Dixon
Mats Ljungman
University of Michigan–Ann Arbor · USUniversity of California, San Diego · USVirginia Tech · US

Funding

CELLULAR AND MOLECULAR BIOLOGY AT MICHIGANT32GM007315 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTHENVEEDU, MANOJKUMAR A · 1985 to 2021
$12.8M
REGULATION OF P53 STABILITY BY SER315 PHOSPHORYLATIONR01CA082376 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LJUNGMAN, MATS · 1999 to 2002
$627k
NCI NIH HHS CA82376NIGMS NIH HHS T32 GM007315
6 · The paper itself

Abstract

backgroundThe evolutionary conserved cyclin-dependent kinase phosphatase hCdc14A has been shown to play potential roles in the regulation of mitotic exit and in the centrosome duplication cycle. We have recently shown that hCdc14A also can interact with the tumor suppressor p53 both in vitro and in vivo and specifically dephosphorylates the ser315 site of p53 in vitro. In this study we developed antibodies against hCdc14A to investigate the expression and regulation of hCdc14A in human tissues and cancer cells.

resultsWe show that hCdc14A is differentially expressed in human tissues and in 75 cancer cell lines examined. Treatments with the histone deacetylase inhibitor TSA, the demethylating agent 5-aza-2'-deoxycytodine or the proteasome inhibitor MG132 significantly induced expression of hCdc14A in cell lines expressing low or undetectable levels of hCdc14A. There was a strong bias for low expression of hCdc14A in cancer cell lines harboring wild-type p53, suggesting that high Cdc14A expression is not compatible with wild-type p53 expression. We present evidence for a role for hCdc14A in the dephosphorylation of the ser315 site of p53 in vivo and that hCdc14A forms a complex with Cdk1/cyclin B during interphase but not during mitosis.

conclusionOur results that hCdc14A is differentially expressed in human cancer cells and that hCdc14A can interact with both p53 and the Cdk1/cyclin B complex may implicate that dysregulation of hCdc14A expression may play a role in carcinogenesis.

Indexed as

Gene Expression Regulation, NeoplasticGenes, p53AzacitidineCDC2 Protein KinaseCell LineCell Line, TumorCyclin BCytidine TriphosphateHumansMitosisModels, BiologicalPhosphoric Monoester HydrolasesPhosphorylationProteasome InhibitorsProtein BindingProtein Tyrosine Phosphatases5-aza-2'-deoxycytidine-5'-triphosphateAzacitidineCDC14A protein, humanCDC2 Protein KinaseCyclin BCytidine TriphosphatePhosphoric Monoester HydrolasesProteasome InhibitorsProtein Tyrosine Phosphatases

Identifiers

PMID16784539
PMCPMC1524803
OpenAlexW2134079593

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.