ArticleeLife2019
An order-to-disorder structural switch activates the FoxM1 transcription factor.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 50 citations in OpenAlex.
- M1-NP1 interfering-peptide inhibits cancer cell proliferation and migration by targeting the transcription factor FOXM1.Journal of pharmaceutical analysis · 2026Article
- Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injury.Signal transduction and targeted therapy · 2025Article
- Tandem association of CLOCK:BMAL1 complexes on DNA enables recruitment of CBP/p300 through multivalent interactions.bioRxiv : the preprint server for biology · 2025Article
- Targeting mCurrent oncology (Toronto, Ont.) · 2025Review
- Review
- Pan-Cancer Upregulation of theGenes · 2025Article
- Article
- FoxM1 promotes TFAM expression and regulates Mitochondrial Dynamics in Glioblastoma cells.Journal of Cancer · 2025Article
- The conformation of FOXM1 homodimers in vivo is crucial for regulating transcriptional activities.Nucleic acids research · 2024Article
- Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- FOXM1, MEK, and CDK4/6: New Targets for Malignant Peripheral Nerve Sheath Tumor Therapy.International journal of molecular sciences · 2023Review
- Development of an interfering peptide M1-20 with potent anti-cancer effects by targeting FOXM1.Cell death & disease · 2023Article
- FOXM1: A small fox that makes more tracks for cancer progression and metastasis.Seminars in cancer biology · 2023Review
- Targeting the oncogenic transcription factor FOXM1 to improve outcomes in all subtypes of breast cancer.Breast cancer research : BCR · 2023Review
- The Role of Polo-Like Kinase 1 in Regulating the Forkhead Box Family Transcription Factors.Cells · 2023Review
- Deciphering the multi-scale, quantitative cis-regulatory code.Molecular cell · 2023Review
- Structural insights into p300 regulation and acetylation-dependent genome organisation.Nature communications · 2022Article
- Targetable vulnerability of deregulated FOXM1/PLK1 signaling axis in diffuse large B cell lymphoma.American journal of cancer research · 2022Article
- A Structural Perspective of Reps from CRESS-DNA Viruses and Their Bacterial Plasmid Homologues.Viruses · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Intrinsically disordered transcription factor transactivation domains (TADs) function through structural plasticity, adopting ordered conformations when bound to transcriptional co-regulators. Many transcription factors contain a negative regulatory domain (NRD) that suppresses recruitment of transcriptional machinery through autoregulation of the TAD. We report the solution structure of an autoinhibited NRD-TAD complex within FoxM1, a critical activator of mitotic gene expression. We observe that while both the FoxM1 NRD and TAD are primarily intrinsically disordered domains, they associate and adopt a structured conformation. We identify how Plk1 and Cdk kinases cooperate to phosphorylate FoxM1, which releases the TAD into a disordered conformation that then associates with the TAZ2 or KIX domains of the transcriptional co-activator CBP. Our results support a mechanism of FoxM1 regulation in which the TAD undergoes switching between disordered and different ordered structures.
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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.