ArticleCytoskeleton (Hoboken, N.J.)2011
Centrosome amplification in CHO and DT40 cells by inactivation of cyclin-dependent kinases.
Article in Cytoskeleton (Hoboken, N.J.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Centrosome amplification promotes cell invasion via cell-cell contact disruption and Rap-1 activation.Journal of cell science · 2023Article
- Vesicular trafficking plays a role in centriole disengagement and duplication.Molecular biology of the cell · 2018Article
- Centrosome Remodelling in Evolution.Cells · 2018Review
- Clinically Applicable Inhibitors Impacting Genome Stability.Molecules (Basel, Switzerland) · 2018Review
- 14-3-3γ Prevents Centrosome Amplification and Neoplastic Progression.Scientific reports · 2016Article
- CDK1 Prevents Unscheduled PLK4-STIL Complex Assembly in Centriole Biogenesis.Current biology : CB · 2016Article
- Centrosome - a promising anti-cancer target.Biologics : targets & therapy · 2016Review
- Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells.Molecular biology of the cell · 2013Article
- PPP1R42, a PP1 binding protein, regulates centrosome dynamics in ARPE-19 cells.Biology of the cell · 2013Article
- Identification of cilia genes that affect cell-cycle progression using whole-genome transcriptome analysis in Chlamydomonas reinhardtti.G3 (Bethesda, Md.) · 2013Article
- Cep63 and cep152 cooperate to ensure centriole duplication.PloS one · 2013Article
- Oscillation of APC/C activity during cell cycle arrest promotes centrosome amplification.Journal of cell science · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
To study the mechanism of centrosome duplication in cycling cells, we established a novel system of multiple centrosome formation in two types of cells: CHO cells treated with RO3306, a Cyclin-dependent kinase 1 (Cdk1) inhibitor and DT40 cells, in which Cdks were knocked out by chemical genetics. Cdk1-inactivated cells initiated DNA replication and centrosome duplication at the onset of S phase. They became arrested at the end of G2, but the centrosome cycle continued to produce supernumerary centrioles/centrosomes without DNA endoreplication in those cells. Centrosomes were amplified in a highly synchronous and reproducible manner: all of them were located next to the nucleus and spread widely apart from each other with several μm in distance. Double knockout of Cdk1 and Cdk2 caused cell cycle arrest at G1/S and centrosomes were no longer duplicated. However, cells continued to grow and increased their volume over 10-fold during 48 hr of culture. Centrosome components, including γ-tubulin and Cep135, were synthesized and accumulated during the arrest, allowing rapid centrosome multiplication upon recovery from the cell cycle arrest or expression of exogenous Plk4 in G1/S cells. Thus centrosome amplification results from the discoordination of the centrosome cycle from the progression of other cell cycle events, which is controlled by different levels of Cdk activities.
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Registered trials
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.