ArticleCell2007
Cdk-inhibitory activity and stability of p27Kip1 are directly regulated by oncogenic tyrosine kinases.
Article in Cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 2 of them syntheses that pooled it.
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
200 citing papers in PubMed, 2 syntheses or guidelines pooled it, 334 citations in OpenAlex.
- Prognostic significance of p27 in colorectal cancer: a meta-analysis and bioinformatics analysis.Frontiers in oncology · 2024Pooled it
- Reciprocal regulation of metabolic and signaling pathways.BMC genomics · 2010Pooled it
- Aromatase inhibition plus/minus Src inhibitor saracatinib (AZD0530) in advanced breast cancer therapy (ARISTACAT): a randomised phase II study.Breast cancer research and treatment · 2023Trial
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
- Cell-cycle targeted cancer therapy: clinical advances, biological gaps, and the emergence of selective CDK4 inhibitors.Journal of hematology & oncology · 2026Review
- CDKN1B (p27/kip1) enhances drug-tolerant persister CTCs by restricting polyploidy following mitotic inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies.Genes & diseases · 2025Review
- Structural Identification of Major Molecular Determinants for Phosphotyrosine Recognition in Tyrosine Kinases Reveals Tumour Promoting and Suppressive Functions.bioRxiv : the preprint server for biology · 2025Article
- ARv7 promotes the escape of prostate cancer cells from androgen deprivation therapy-induced senescence by mediating the SKP2/p27 axis.BMC biology · 2025Article
- p27Cells · 2025Article
- Ruthenium(II) Complex with 1-Hydroxy-9,10-Anthraquinone Inhibits Cell Cycle Progression at G0/G1 and Induces Apoptosis in Melanoma Cells.Pharmaceuticals (Basel, Switzerland) · 2025Article
- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
- The CDK4/6 inhibitor revolution - a game-changing era for breast cancer treatment.Nature reviews. Clinical oncology · 2024Review
- Complement C7 and clusterin form a complex in circulation.Frontiers in immunology · 2024Article
- Article
- Coordinated activation of c-Src and FOXM1 drives tumor cell proliferation and breast cancer progression.The Journal of clinical investigation · 2023Article
- Commentary: locating the restriction point.Cell division · 2023Article
- Emerging approaches to CDK inhibitor development, a structural perspective.RSC chemical biology · 2023Article
- p27International journal of molecular sciences · 2022Article
- The SKP2-p27 axis defines susceptibility to cell death upon CHK1 inhibition.Molecular oncology · 2022Article
140 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
p27Kip1 controls cell proliferation by binding to and regulating the activity of cyclin-dependent kinases (Cdks). Here we show that Cdk inhibition and p27 stability are regulated through direct phosphorylation by tyrosine kinases. A conserved tyrosine residue (Y88) in the Cdk-binding domain of p27 can be phosphorylated by the Src-family kinase Lyn and the oncogene product BCR-ABL. Y88 phosphorylation does not prevent p27 binding to cyclin A/Cdk2. Instead, it causes phosphorylated Y88 and the entire inhibitory 3(10)-helix of p27 to be ejected from the Cdk2 active site, thus restoring partial Cdk activity. Importantly, this allows Y88-phosphorylated p27 to be efficiently phosphorylated on threonine 187 by Cdk2 which in turn promotes its SCF-Skp2-dependent degradation. This direct link between transforming tyrosine kinases and p27 may provide an explanation for Cdk kinase activities observed in p27 complexes and for premature p27 elimination in cells that have been transformed by activated tyrosine kinases.
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What OpenQuestion holds
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.