ReviewOncogene2005
Getting in and out of mitosis with Polo-like kinase-1.
Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 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
125 citing papers in PubMed, 270 citations in OpenAlex.
- A phase II/III randomized study to compare the efficacy and safety of rigosertib plus gemcitabine versus gemcitabine alone in patients with previously untreated metastatic pancreatic cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2015Trial
- TOPBP1-PLK1 interaction preserves genome integrity during mitosis.Nucleic acids research · 2026Article
- RIOK2 kinase regulates the translocation of the FADD-RIPK1-Caspase-8 complex to the ER and the cleavage of Gasdermin D to drive pyroptosis.Nature communications · 2025Article
- Cyanobacterial scytonemin, a potential photoprotective natural pigment: biomedical, industrial and environmental applications.Archives of microbiology · 2025Review
- Polo-like Kinase 1 Expression as a Biomarker in Colorectal Cancer: A Retrospective Two-Center Study.Biomedicines · 2024Article
- METTL16-mediated N6-methyladenosine modification of Soga1 enables proper chromosome segregation and chromosomal stability in colorectal cancer.Cell proliferation · 2024Article
- Icaritin inhibits PLK1 to activate DNA damage response in NK/T cell lymphoma and increases sensitivity to GELOX regime.Molecular therapy oncolytics · 2022Article
- Salt-inducible kinase 3 protects tumor cells from cytotoxic T-cell attack by promoting TNF-induced NF-κB activation.Journal for immunotherapy of cancer · 2022Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Rigosertib and Cholangiocarcinoma: A Cell Cycle Affair.International journal of molecular sciences · 2021Article
- Dynamic regulation of mitotic ubiquitin ligase APC/C by coordinated Plx1 kinase and PP2A phosphatase action on a flexible Apc1 loop.The EMBO journal · 2021Article
- Cell Cycle Control: A System of Interlinking Oscillators.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Development of a Polo-like Kinase-1 Polo-Box Domain Inhibitor as a Tumor Growth Suppressor in Mice Models.Journal of medicinal chemistry · 2020Article
- Targeting the ABC transporter ABCB5 sensitizes glioblastoma to temozolomide-induced apoptosis through a cell-cycle checkpoint regulation mechanism.The Journal of biological chemistry · 2020Article
- Article
- Identification of inhibitors of the polo-box domain of polo-like kinase 1 from natural and semisynthetic compounds.Investigational new drugs · 2020Article
- PLK1 targets NOTCH1 during DNA damage and mitotic progression.The Journal of biological chemistry · 2019Article
- Design of Peptidomimetic Functionalized Cholesterol Based Lipid Nanoparticles for Efficient Delivery of Therapeutic Nucleic Acids.Molecules (Basel, Switzerland) · 2019Article
- Dissecting phenotypic responses of the druggable targetome in cancers.Scientific reports · 2019Article
- A requirement of Polo-like kinase 1 in murine embryonic myogenesis and adult muscle regeneration.eLife · 2019Article
65 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research in different species has shown that Polo-like kinases are essential for successful cell division. In human cells, Polo-like kinase-1 (Plk1) has been implicated in the regulation of different processes, including mitotic entry, spindle formation and cytokinesis. Recently, a range of new downstream targets of Plk1 has been identified, as well as a molecular mechanism that explains recruitment of Plk1 to potential substrate proteins through its polo-box domain. On the basis of these reports, we discuss possible mechanisms by which Polo-like kinases can exert their multiple functions during mitosis. Polo-like kinases also function in DNA damage checkpoints. Plk1 has been shown to be a target of the G2 DNA damage checkpoint, while Cdc5, the Polo-like kinase in Saccharomyces cerevisiae, has long been known to be required for adaptation to persistent DNA damage. Just recently, a similar requirement for Polo-like kinases during checkpoint adaptation was demonstrated in multicellular organisms. Moreover, Plk1 was also shown to be required for checkpoint recovery following checkpoint inactivation, that is, in cells where the damage is completely repaired. Thus, Plk1 appears to play a role at multiple points during a restart of the cell cycle following DNA damage. Based on these novel observations, we discuss possible consequences of using Plk1 as a target in anticancer strategies.
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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.