Evidence map›Paper›PMID 17438528›Full record

ArticleOncogene2007

Centriole overduplication through the concurrent formation of multiple daughter centrioles at single maternal templates.

A Duensing, Y Liu, S A Perdreau, J Kleylein-Sohn, E A Nigg, S Duensing

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
  2. The E3 ligase Poe promotes Pericentrin degradation.Molecular biology of the cell · 2023
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  14. Precision Revisited: Targeting Microcephaly Kinases in Brain Tumors.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Article
  17. Ubiquitin, the centrosome, and chromosome segregation.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  18. Centrosome amplification, chromosomal instability and cancer: mechanistic, clinical and therapeutic issues.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

A DuensingDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. duensing@pitt.edu
Y Liu
S A Perdreau
J Kleylein-Sohn
E A Nigg
S Duensing
UPMC Hillman Cancer Center · USMax Planck Institute of Biochemistry · DEUniversity of Pittsburgh · US

Funding

Genomic instability induced by the HPV-16 E7 oncoproteinR01CA112598 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DUENSING, STEFAN · 2005 to 2009
$1.1M
NCI NIH HHS R01 CA112598
6 · The paper itself

Abstract

Abnormal centrosome numbers are detected in virtually all cancers. The molecular mechanisms that underlie centrosome amplification, however, are poorly characterized. Based on the model that each maternal centriole serves as a template for the formation of one and only one daughter centriole per cell division cycle, the prevailing view is that centriole overduplication arises from successive rounds of centriole reproduction. Here, we provide evidence that a single maternal centriole can concurrently generate multiple daughter centrioles. This mechanism was initially identified in cells treated with the peptide vinyl sulfone proteasome inhibitor Z-L(3)VS. We subsequently found that the formation of more than one daughter at maternal centrioles requires cyclin E/cyclin-dependent kinase 2 as well as Polo-like kinase 4 and that overexpression of these proteins mimics this phenotype in the absence of a proteasome inhibitor. Moreover, we show that the human papillomavirus type 16 E7 oncoprotein stimulates aberrant daughter centriole numbers in part through the formation of more than one daughter centriole at single maternal templates. These results help to explain how oncogenic stimuli can rapidly induce abnormal centriole numbers within a single cell-division cycle and provide insights into the regulation of centriole duplication.

Indexed as

Cell LineCentriolesCyclin-Dependent Kinase 2Cyclin EHumansMicroscopy, ElectronMitosisOligopeptidesOncogene Proteins, ViralPapillomavirus E7 ProteinsProtease InhibitorsProteasome Endopeptidase ComplexProteasome InhibitorsProtein Serine-Threonine KinasesSpindle ApparatusSulfonescarboxybenzyl-leucyl-leucyl-leucine vinyl sulfoneCyclin-Dependent Kinase 2Cyclin EOligopeptidesoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsPLK4 protein, humanProtease InhibitorsProteasome Endopeptidase ComplexProteasome InhibitorsProtein Serine-Threonine KinasesSulfones

Identifiers

PMID17438528
PMCPMC2586811
OpenAlexW1995947461

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.