ReviewOncogene2005
Sak/Plk4 and mitotic fidelity.
Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- In vitro approaches to study centriole and cilium function in early mouse embryogenesis.Life science alliance · 2026Article
- 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
- Treatment of glioblastoma with tumor-specific amplitude-modulated radiofrequency electromagnetic fields.Oncotarget · 2025Article
- Inhibition of Aberrantly Overexpressed Polo-like Kinase 4 Is a Potential Effective Treatment for DNA Damage Repair-Deficient Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- PLK4 is upregulated in prostate cancer and its inhibition reduces centrosome amplification and causes senescence.The Prostate · 2022Article
- Role of Polo-like Kinases Plk1 and Plk4 in the Initiation of Centriole Duplication-Impact on Cancer.Cells · 2022Review
- Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signaling pathway in bladder cancer.FEBS open bio · 2021Article
- Molecular interactions of miR-338 during tumor progression and metastasis.Cellular & molecular biology letters · 2021Review
- Polo-Like Kinase 4's Critical Role in Cancer Development and Strategies for Plk4-Targeted Therapy.Frontiers in oncology · 2021Review
- A cis-eQTL genetic variant in PLK4 confers high risk of hepatocellular carcinoma.Cancer medicine · 2019Article
- Polo-like kinase 4 mediates epithelial-mesenchymal transition in neuroblastoma via PI3K/Akt signaling pathway.Cell death & disease · 2018Article
- Analysis of centrosome and DNA damage response in PLK4 associated Seckel syndrome.European journal of human genetics : EJHG · 2017Article
- PLK4 phosphorylation of CP110 is required for efficient centriole assembly.Cell cycle (Georgetown, Tex.) · 2017Article
- Human male infertility and its genetic causes.Reproductive medicine and biology · 2017Review
- Activity of the novel polo-like kinase 4 inhibitor CFI-400945 in pancreatic cancer patient-derived xenografts.Oncotarget · 2017Article
- The PLK4-STIL-SAS-6 module at the core of centriole duplication.Biochemical Society transactions · 2016Review
- Hepatocellular carcinoma mouse models: Hepatitis B virus-associated hepatocarcinogenesis and haploinsufficient tumor suppressor genes.World journal of gastroenterology · 2016Review
- Loss of KLF14 triggers centrosome amplification and tumorigenesis.Nature communications · 2015Article
- Binding of STIL to Plk4 activates kinase activity to promote centriole assembly.The Journal of cell biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sak/Plk4 differs from other polo-like kinases in having only a single polo box, which assumes a novel dimer fold that localizes to the nucleolus, centrosomes and the cleavage furrow. Sak expression increases gradually in S through M phase, and Sak is destroyed by APC/C dependent proteolysis. Sak-deficient mouse embryos arrest at E7.5 and display an increased incidence of apoptosis and anaphase arrest. Sak(+/-) mice are haploinsufficient for tumor suppression, with spontaneous tumors developing primarily in the liver with advanced age. During liver regeneration following partial hepatectomy, Sak(+/-) hepatocytes display a delay in reaching the first M phase, multipolar spindles, disorganized tissue morphology and loss of acuity for cyclin B1 expression. Similarly, Sak(+/-) MEF cells proliferate slowly, and show a high incidence of centrosome hyper-amplification. We suggest that Sak provides feedback to cell cycle regulators, and thereby precision to the switch-like transitions of centrosome duplication and exit-from-mitosis. Sak binds to p53, and studies are underway to provide a molecular context for the Sak-p53 interaction. Animal models of haploinsufficiency and more comprehensive models of cell cycle regulation should contribute to improvements in cancer risk assessment and novel therapies.
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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.