ArticleNature cell biology2017
G1 cyclins link proliferation, pluripotency and differentiation of embryonic stem cells.
Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 132 citations in OpenAlex.
- Direct Mapping of CDK2 Substrates in Embryonic Stem Cells Uncovers an AP-Site Repair Mechanism via HMCES Phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- Fine-tuning ERK activity enables proliferation-differentiation balance during lineage specification of human embryonic stem cells.PLoS biology · 2026Article
- A non-coding role for trypanosome VSG transcripts in allelic exclusion.Nucleic acids research · 2025Article
- ATR regulates OCT4 phosphorylation and safeguards human naïve pluripotency.Scientific reports · 2025Article
- Article
- Genes as Genome Stabilizers in Pluripotent Stem Cells.Advances in experimental medicine and biology · 2025Review
- Coupling of stemness maintenance with cell cycle control in stem cells.Frontiers in cell and developmental biology · 2025Review
- Transcriptomic Changes in Human Tonsil-Derived Mesenchymal Stem Cells Across Culture Passages.Genes · 2024Article
- NaV1.1 contributes to the cell cycle of human mesenchymal stem cells by regulating AKT and CDK2.Journal of cell science · 2024Article
- A live single-cell reporter system reveals drug-induced plasticity of a cancer stem cell-like population in cholangiocarcinoma.Scientific reports · 2024Article
- Protein restriction during pregnancy alters Cdkn1c silencing, dopamine circuitry and offspring behaviour without changing expression of key neuronal marker genes.Scientific reports · 2024Article
- Developmental progression continues during embryonic diapause in the roe deer.Communications biology · 2024Article
- Molecular subtyping and characterization of clear cell renal cell carcinoma by tumor differentiation trajectories.iScience · 2023Article
- Transcriptional repression upon S phase entry protects genome integrity in pluripotent cells.Nature structural & molecular biology · 2023Article
- Review
- CDK6 is activated by the atypical cyclin I to promote E2F-mediated gene expression and cancer cell proliferation.Molecular oncology · 2023Article
- Mammalian CDC14 phosphatases control exit from stemness in pluripotent cells.The EMBO journal · 2023Article
- Transmembrane protein 121 as a novel inhibitor of cervical cancer metastasis.Experimental and therapeutic medicine · 2022Article
- Review
- Targeting CDK4 and CDK6 in cancer.Nature reviews. Cancer · 2022Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.
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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.