Evidence map›Paper›PMID 22892665›Full record

ReviewCellular and molecular life sciences : CMLS2013

Show me your license, please: deregulation of centriole duplication mechanisms that promote amplification.

Christopher W Brownlee, Gregory C Rogers

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Centrosome dysfunction: a link between senescence and tumor immunity.Signal transduction and targeted therapy · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Regulation of the centrosome cycle.Molecular & cellular oncology · 2016
    Review
  9. Centrosomes in the DNA damage response--the hub outside the centre.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  10. Article
  11. Article
  12. Causes and consequences of centrosome abnormalities in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  13. Exploring the evolutionary history of centrosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Christopher W BrownleeDepartment of Cellular and Molecular Medicine, Arizona Cancer Center, University of Arizona, Tucson, AZ 85724, USA.
Gregory C Rogers
University of Arizona · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
NCI NIH HHS P30 CA023074NCI NIH HHS P30 CA23074NCI NIH HHS P50 CA095060NCI NIH HHS P50 CA95060
6 · The paper itself

Abstract

Centrosomes are organelles involved in generating and organizing the interphase microtubule cytoskeleton, mitotic spindles and cilia. At the centrosome core are a pair of centrioles, structures that act as the duplicating elements of this organelle. Centrioles function to recruit and organize pericentriolar material which nucleates microtubules. While centrioles are relatively simple in construction, the mechanics of centriole biogenesis remain an important yet poorly understood process. More mysterious still are the regulatory mechanisms that oversee centriole assembly. The fidelity of centriole duplication is critical as defects in either the assembly or number of centrioles promote aneuploidy, primary microcephaly, birth defects, ciliopathies and tumorigenesis. In addition, some pathogens employ mechanisms to promote centriole overduplication to the detriment of the host cell. This review summarizes our current understanding of this important topic, highlighting the need for further study if new therapeutics are to be developed to treat diseases arising from defects of centrosome duplication.

Indexed as

Models, BiologicalAnimalsCell CycleCell Cycle ProteinsCentriolesDrosophila melanogasterHumansMitosisProtein Serine-Threonine KinasesCell Cycle ProteinsPLK4 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID22892665
PMCPMC11113234
OpenAlexW2090077882

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.