ArticleOncogene2007
Direct evidence for the role of centrosomally localized p53 in the regulation of centrosome duplication.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 88 citations in OpenAlex.
- STIL Overexpression Is Associated with Chromosomal Numerical Abnormalities in Non-Small-Cell Lung Carcinoma Through Centrosome Amplification.Current oncology (Toronto, Ont.) · 2024Article
- Targeting TACC3 represents a novel vulnerability in highly aggressive breast cancers with centrosome amplification.Cell death and differentiation · 2023Article
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- CK1 Is a Druggable Regulator of Microtubule Dynamics and Microtubule-Associated Processes.Cancers · 2022Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Review
- Centrosome dysfunction: a link between senescence and tumor immunity.Signal transduction and targeted therapy · 2020Review
- Moonlighting in Mitosis: Analysis of the Mitotic Functions of Transcription and Splicing Factors.Cells · 2020Review
- Review
- Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis.Journal of virology · 2020Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- p53 mitotic centrosome localization preserves centrosome integrity and works as sensor for the mitotic surveillance pathway.Cell death & disease · 2019Article
- HER2, chromosome 17 polysomy and DNA ploidy status in breast cancer; a translational study.Scientific reports · 2019Article
- Irradiation induces p53 loss of heterozygosity in breast cancer expressing mutant p53.Communications biology · 2019Article
- Increased Genetic Instability and Accelerated Progression of Colitis-Associated Colorectal Cancer through Intestinal Epithelium-specific Deletion ofMolecular cancer research : MCR · 2019Article
- A look into centrosome abnormalities in colon cancer cells, how they arise and how they might be targeted therapeutically.Biochemical pharmacology · 2018Review
- DDX3 localizes to the centrosome and prevents multipolar mitosis by epigenetically and translationally modulating p53 expression.Scientific reports · 2017Article
- Functional Roles of E6 and E7 Oncoproteins in HPV-Induced Malignancies at Diverse Anatomical Sites.Cancers · 2016Review
- Genome Stability Requires p53.Cold Spring Harbor perspectives in medicine · 2016Review
- Over-expression of Plk4 induces centrosome amplification, loss of primary cilia and associated tissue hyperplasia in the mouse.Open biology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal amplification of centrosomes is the major cause of mitotic defects and chromosome instability in cancer cells. Centrosomes duplicate once in each cell cycle, and abrogation of the regulatory mechanism underlying centrosome duplication leads to centrosome amplification. p53 tumor suppressor protein is involved in the regulation of centrosome duplication: loss of p53 as well as expression of certain p53 mutants result in deregulated centrosome duplication and centrosome amplification. p53 at least in part depends on its transactivation function to control centrosome duplication, primarily via upregulation of p21 cyclin-dependent kinase (CDK) inhibitor, which prevents untimely activation of CDK2/cyclin E, a key initiator of centrosome duplication. However, numerous studies have shown the presence of p53 at centrosomes, yet the role of the centrosomally localized p53 in the regulation of centrosome duplication had been enigmatic. Here, we comparatively examined wild-type p53 and p53 mutants that are transactivation(+)/centrosome-binding(-), transactivation(-)/centrosome-binding(+) and transactivation(-)/centrosome-binding(-) for their abilities to control centrosome duplication. We found that the transactivation(+)/centrosome-binding(-) and transactivation(-)/centrosome-binding(+) mutants suppress centrosome duplication only partially compared with wild-type p53. Moreover, the transactivation(-)/centrosome-binding(-) mutant almost completely lost the ability to suppress centrosome duplication. These observations provide direct evidence for the centrosomally localized p53 to participate in the regulation of centrosome duplication in a manner independent of its transactivation function in addition to its transactivation-dependent regulation of centrosome duplication.
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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.