ArticleCell2016
Irreversible APC(Cdh1) Inactivation Underlies the Point of No Return for Cell-Cycle Entry.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 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
166 citing papers in PubMed.
- WEE1 opposes APC/CNature · 2026Article
- Targeting casein kinase 1α-mediated FADD phosphorylation restores sensitivity in select CDK4/6 inhibitor-resistant breast cancer models.The Journal of clinical investigation · 2026Article
- Diverse Roles of Cohesin in Chromosome Dynamics and Stem Cells.Biotech (Basel (Switzerland)) · 2026Review
- A Function-Centric Framework for Mitochondrial Quality Control.Biomolecules · 2026Review
- CDC7 and APC/CNature communications · 2026Article
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
- Replicative senescence induction in single cells is not predicted by telomere length, dysfunction, or oxidation.iScience · 2026Article
- Protocol for iterative indirect immunofluorescence imaging of frozen mouse intestinal tissues.STAR protocols · 2026Article
- Asymmetric division in a two-cell-like state rejuvenates embryonic stem cells.Cell research · 2026Article
- Cell cycle criticality as a mechanism for robust cell population control.Molecular systems biology · 2026Article
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Cell Population Dynamics Informed by Cell-Cycle Regulation: A Deterministic Modeling Toolkit.Computational and structural biotechnology journal · 2026Review
- CDH1 Orchestrates Anabolic Events to Promote Cell Cycle Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrative Proteogenomics and Forward Genetics Reveal a Novel Mitotic Vulnerability in Triple-Negative Breast Cancer.Cancer discovery · 2025Article
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.Cell reports · 2025Article
- Article
- Temporal control of human DNA replication licensing by CDK4/6-RB signalling and chemical genetics.Nature communications · 2025Article
- Recent advances in spying on cell signaling with fluorescent biosensors.Current opinion in cell biology · 2025Review
- Discovery of potent and selective PROTACs for the protein kinase LZK for the treatment of head and neck cancer.The Journal of biological chemistry · 2025Article
- Article
106 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
5 authors.
Funding
Abstract
Proliferating cells must cross a point of no return before they replicate their DNA and divide. This commitment decision plays a fundamental role in cancer and degenerative diseases and has been proposed to be mediated by phosphorylation of retinoblastoma (Rb) protein. Here, we show that inactivation of the anaphase-promoting complex/cyclosome (APC(Cdh1)) has the necessary characteristics to be the point of no return for cell-cycle entry. Our study shows that APC(Cdh1) inactivation is a rapid, bistable switch initiated shortly before the start of DNA replication by cyclin E/Cdk2 and made irreversible by Emi1. Exposure to stress between Rb phosphorylation and APC(Cdh1) inactivation, but not after APC(Cdh1) inactivation, reverted cells to a mitogen-sensitive quiescent state, from which they can later re-enter the cell cycle. Thus, APC(Cdh1) inactivation is the commitment point when cells lose the ability to return to quiescence and decide to progress through the cell cycle.
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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.