ArticleThe Journal of cell biology2011
The Protein Phosphatase 2A regulatory subunit Twins stabilizes Plk4 to induce centriole amplification.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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.
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.
Who cites it
66 citing papers in PubMed, 109 citations in OpenAlex.
- The Centriole Biogenesis Cycle: Temporal Mechanisms, Autonomy and Coupling to the Cell Cycle and Other Cellular Clocks.Advances in experimental medicine and biology · 2026Review
- Review
- Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.Carcinogenesis · 2025Review
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- A disease-associated PPP2R3C-MAP3K1 phospho-regulatory module controls centrosome function.Current biology : CB · 2024Article
- PP2A-B55 phosphatase counteracts Ki-67-dependent chromosome individualization during mitosis.Cell reports · 2024Article
- A disease-associated PPP2R3C-MAP3K1 phospho-regulatory module controls centrosome function.bioRxiv : the preprint server for biology · 2024Article
- Generating CRISPR-edited clonal lines of culturedBiology methods & protocols · 2024Article
- Site-specific phosphorylation of ZYG-1 regulates ZYG-1 stability and centrosome number.iScience · 2023Article
- Towards understanding centriole elimination.Open biology · 2023Review
- Polo-like kinase 4 homodimerization and condensate formation regulate its own protein levels but are not required for centriole assembly.Molecular biology of the cell · 2023Article
- Plk4 Is a Novel Substrate of Protein Phosphatase 5.International journal of molecular sciences · 2023Article
- Article
- Balancing the scales: fine-tuning Polo-like kinase 4 to ensure proper centriole duplication.Genes & development · 2022Review
- Daughter centrioles assemble preferentially towards the nuclear envelope inOpen biology · 2022Article
- Identification of GOLPH3 Partners inCells · 2021Article
- Chromosome Unipolar Division and Low Expression ofInsects · 2021Article
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- Phospho-regulation of mitotic spindle assembly.Cytoskeleton (Hoboken, N.J.) · 2020Review
- FAM46C/TENT5C functions as a tumor suppressor through inhibition of Plk4 activity.Communications biology · 2020Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Centriole duplication is a tightly regulated process that must occur only once per cell cycle; otherwise, supernumerary centrioles can induce aneuploidy and tumorigenesis. Plk4 (Polo-like kinase 4) activity initiates centriole duplication and is regulated by ubiquitin-mediated proteolysis. Throughout interphase, Plk4 autophosphorylation triggers its degradation, thus preventing centriole amplification. However, Plk4 activity is required during mitosis for proper centriole duplication, but the mechanism stabilizing mitotic Plk4 is unknown. In this paper, we show that PP2A (Protein Phosphatase 2A(Twins)) counteracts Plk4 autophosphorylation, thus stabilizing Plk4 and promoting centriole duplication. Like Plk4, the protein level of PP2A's regulatory subunit, Twins (Tws), peaks during mitosis and is required for centriole duplication. However, untimely Tws expression stabilizes Plk4 inappropriately, inducing centriole amplification. Paradoxically, expression of tumor-promoting simian virus 40 small tumor antigen (ST), a reported PP2A inhibitor, promotes centrosome amplification by an unknown mechanism. We demonstrate that ST actually mimics Tws function in stabilizing Plk4 and inducing centriole amplification.
Indexed as
Identifiers
What OpenQuestion holds
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.