ArticleNature cell biology2008
Plk1-dependent phosphorylation of FoxM1 regulates a transcriptional programme required for mitotic progression.
Article in Nature cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 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
252 citing papers in PubMed, 354 citations in OpenAlex.
- Single-cell analysis identifies TOP2α as a critical regulator of G2/M entry and differentiation-dependent productive HPV replication.bioRxiv : the preprint server for biology · 2026Article
- FOXM1-associated melanoma stratification: integrated multi-omics and experimental validation reveal prognostic significance and therapeutic potential.BMC cancer · 2026Article
- Review
- SIRT2 antagonizes MOF function during mitotic entry.Science advances · 2026Article
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- M1-NP1 interfering-peptide inhibits cancer cell proliferation and migration by targeting the transcription factor FOXM1.Journal of pharmaceutical analysis · 2026Article
- SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts.Redox biology · 2026Article
- Targeting Prolyl 3-hydroxylase 1 inhibits pancreatic cancer progression and macrophage immunity.Nature communications · 2026Article
- FOXM1 induces therapy resistance and inhibits apoptosis in a variety of human cancers.Cell death & disease · 2026Review
- The role of MELK in cancer: mechanisms and therapeutic options.Frontiers in oncology · 2026Review
- PLK1/FOXM1-associated tumor-cell state and macrophage-related immune features in endometrial cancer.Frontiers in oncology · 2026Article
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injury.Signal transduction and targeted therapy · 2025Article
- Polo-like kinase 1 maintains transcription and chromosomal accessibility during mitosis.Molecular biology of the cell · 2025Article
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- Polo-Like Kinase 1 Expression in Colorectal Cancer: Association With RAS Mutations.Cancer science · 2025Article
- ASPM mediates nuclear entrapment of FOXM1 via liquid-liquid phase separation to promote progression of hepatocarcinoma.Genome biology · 2025Article
- Polo-like kinase inhibitors increase AAV production by halting cell cycle progression.Molecular therapy. Methods & clinical development · 2025Article
- Transcriptome Analysis of Canine Histiocytic Sarcoma Tumors and Cell Lines Reveals Multiple Targets for Therapy.Cancers · 2025Article
- The Functional Transcriptomic Landscape Informs Therapeutic Strategies in Multiple Myeloma.Cancer research · 2025Article
192 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Proper control of entry into and progression through mitosis is essential for normal cell proliferation and the maintenance of genome stability. The mammalian mitotic kinase Polo-like kinase 1 (Plk1) is involved in multiple stages of mitosis5. Here we report that Forkhead Box M1 (FoxM1), a substrate of Plk1, controls a transcriptional programme that mediates Plk1-dependent regulation of cell-cycle progression. The carboxy-terminal domain of FoxM1 binds Plk1, and phosphorylation of two key residues in this domain by Cdk1 is essential for Plk1-FoxM1 interaction. Formation of the Plk1-FoxM1 complex allows for direct phosphorylation of FoxM1 by Plk1 at G2/M and the subsequent activation of FoxM1 activity, which is required for expression of key mitotic regulators, including Plk1 itself. Thus, Plk1-dependent regulation of FoxM1 activity provides a positive-feedback loop ensuring tight regulation of transcriptional networks essential for orderly mitotic progression.
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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.