ArticleeLife2020
Stress-mediated exit to quiescence restricted by increasing persistence in CDK4/6 activation.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
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Who cites it
59 citing papers in PubMed, 93 citations in OpenAlex.
- Disruption of CDK4/6-RARα-NF-κB axis attenuates senescence-associated inflammation and improves function during aging and following chemotherapy.Nature aging · 2026Article
- Article
- Ubiquitin-dependent degradation of p27Kip1 and p21Waf1/Cip1 by AMBRA1 ensures G1 and S phase progression and limits replication stress.Nucleic acids research · 2026Article
- Chromatin association promotes UBR5-mediated degradation of Rb.bioRxiv : the preprint server for biology · 2026Article
- Cyclin-E/A/CDK1/2 Kinetic Landscapes Drive Cell Cycle Phase-Specific Progression and Guide Cyclin-E Degradation Strategy.Journal of chemical information and modeling · 2026Article
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Identification and inhibition of the Cyclin D Rb-docking interface that drives cell division.bioRxiv : the preprint server for biology · 2026Article
- Article
- Inactivation of CDK4/6, CDK2, and ERK in G1-phase triggers differentiation commitment.Communications biology · 2025Article
- Dual targeting of CDK4/6 and CDK7 augments tumor response and antitumor immunity in breast cancer models.The Journal of clinical investigation · 2025Article
- Therapeutic benefits of maintaining CDK4/6 inhibitors and incorporating CDK2 inhibitors beyond progression in breast cancer.bioRxiv : the preprint server for biology · 2025Article
- Bexarotene Promotes Neuroblastoma SH-SY5Y Cell Differentiation to Mature Neurons with Decreased Proliferation.Molecular neurobiology · 2025Article
- Oncogenic YAP sensitizes cells to CHK1 inhibition via CDK4/6 driven G1 acceleration.EMBO reports · 2025Article
- E2F activity determines mitosis versus whole-genome duplication in G2-arrested cells.Nature communications · 2025Article
- Capturing CDKs in action: Live-cell biosensors pioneer the new frontiers in cell cycle research.Cell structure and function · 2025Review
- Tumor Suppressors Condition Differential Responses to the Selective CDK2 Inhibitor BLU-222.Cancer research · 2025Article
- Spherical Manifolds Capture Drug-Induced Changes in Tumor Cell Cycle Behavior.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- Molecular Spies in Action: Genetically Encoded Fluorescent Biosensors Light up Cellular Signals.Chemical reviews · 2024Review
- Palbociclib as an Antitumor Drug: A License to Kill.Molecules (Basel, Switzerland) · 2024Review
- Aurora B inhibitors promote RB hypophosphorylation and senescence independent of p53-dependent CDK2/4 inhibition.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Mammalian cells typically start the cell-cycle entry program by activating cyclin-dependent protein kinase 4/6 (CDK4/6). CDK4/6 activity is clinically relevant as mutations, deletions, and amplifications that increase CDK4/6 activity contribute to the progression of many cancers. However, when CDK4/6 is activated relative to CDK2 remained incompletely understood. Here, we developed a reporter system to simultaneously monitor CDK4/6 and CDK2 activities in single cells and found that CDK4/6 activity increases rapidly before CDK2 activity gradually increases, and that CDK4/6 activity can be active after mitosis or inactive for variable time periods. Markedly, stress signals in G1 can rapidly inactivate CDK4/6 to return cells to quiescence but with reduced probability as cells approach S phase. Together, our study reveals a regulation of G1 length by temporary inactivation of CDK4/6 activity after mitosis, and a progressively increasing persistence in CDK4/6 activity that restricts cells from returning to quiescence as cells approach S phase.
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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.