ReviewNucleic acids research2020
A unified model for the G1/S cell cycle transition.
Review in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
114 citing papers in PubMed, 187 citations in OpenAlex.
- Lidocaine enhances antitumor effects of sorafenib and GW5074 in colorectal cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Dual inhibitors of CDK2 and TRKA kinases: design, synthesis, antiproliferative activity and molecular modeling of novel pyrazolopyrimidine derivatives.RSC advances · 2026Article
- Dual-target carbonic anhydrase inhibitors in cancer therapy: progress, challenges, and opportunities.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- A novel small molecule inhibitor targeting KHSRP methylation suppresses colon cancer progression.Acta pharmaceutica Sinica. B · 2026Article
- CDK4/6 Inhibition Induces CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SDC4 silencing promotes cell cycle arrest at the restriction point (R point) in anoikis-resistant endothelial cells.Cytotechnology · 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
- Mathematical analysis of G1/S sub-networks in hematopoietic proliferation: Sequential and lineage-specific activation.iScience · 2026Article
- Article
- TRV130 inhibits colon cancer progression via suppressing the Hedgehog signaling pathway: in vitro and in vivo evidence.Hereditas · 2026Article
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Repurposing Cell Cycle Oscillators for Multiciliated Cell Differentiation.Advances in experimental medicine and biology · 2026Review
- CDK2-Mediated Phosphorylation ofResearch (Washington, D.C.) · 2026Article
- Evaluating the synergistic effects of cisplatin and tamoxifen in canine osteosarcoma cells.Frontiers in veterinary science · 2026Article
- Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapy.Cell communication and signaling : CCS · 2025Article
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025Review
- An inhibitor of UHM splicing factors exerts anti-leukemic activity by altering cell cycle progression and reducing lysosome acidification.Cellular signalling · 2025Article
- A pentacyclic triterpene tormentic acid inhibits the proliferation and migration of pancreatic ductal adenocarcinoma cells.Translational cancer research · 2025Article
- A novel liphagal analog, IIIM-321, induces apoptosis in melanoma cells via autophagy modulation and PI3K/MAPK pathway inhibition.Cytotechnology · 2025Article
54 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
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Efficient S phase entry is essential for development, tissue repair, and immune defences. However, hyperactive or expedited S phase entry causes replication stress, DNA damage and oncogenesis, highlighting the need for strict regulation. Recent paradigm shifts and conflicting reports demonstrate the requirement for a discussion of the G1/S transition literature. Here, we review the recent studies, and propose a unified model for the S phase entry decision. In this model, competition between mitogen and DNA damage signalling over the course of the mother cell cycle constitutes the predominant control mechanism for S phase entry of daughter cells. Mitogens and DNA damage have distinct sensing periods, giving rise to three Commitment Points for S phase entry (CP1-3). S phase entry is mitogen-independent in the daughter G1 phase, but remains sensitive to DNA damage, such as single strand breaks, the most frequently-occurring lesions that uniquely threaten DNA replication. To control CP1-3, dedicated hubs integrate the antagonistic mitogenic and DNA damage signals, regulating the stoichiometric cyclin: CDK inhibitor ratio for ultrasensitive control of CDK4/6 and CDK2. This unified model for the G1/S cell cycle transition combines the findings of decades of study, and provides an updated foundation for cell cycle research.
Indexed as
Identifiers
What Socratic 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 Socratic graph.