ArticleMolecular biology of the cell2017
Cell-cycle transitions: a common role for stoichiometric inhibitors.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 29 citations in OpenAlex.
- Chromosome segregation synchrony in S. pombe is noise limited and arises without positive feedback.The Journal of cell biology · 2026Article
- Chromosome segregation synchrony inbioRxiv : the preprint server for biology · 2026Article
- Mechanistic origins of temperature scaling in the early embryonic cell cycle.Nature communications · 2025Article
- Kinetic modelling reveals the presence of multistability in normal and stressful conditions in translational initiation mechanism.PloS one · 2025Article
- Newton's cradle: Cell cycle regulation by two mutually inhibitory oscillators.Mathematical biosciences · 2024Article
- From biological data to oscillator models using SINDy.iScience · 2024Article
- Cell Fate following Irradiation of MDA-MB-231 and MCF-7 Breast Cancer Cells Pre-Exposed to the Tetrahydroisoquinoline Sulfamate Microtubule Disruptor STX3451.Molecules (Basel, Switzerland) · 2022Article
- Cell cycle-independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry.The Journal of cell biology · 2022Article
- MicroRNA governs bistable cell differentiation and lineage segregation via a noncanonical feedback.Molecular systems biology · 2021Article
- RNA Helicases as Shadow Modulators of Cell Cycle Progression.International journal of molecular sciences · 2021Review
- Bistable, Biphasic Regulation of PP2A-B55 Accounts for the Dynamics of Mitotic Substrate Phosphorylation.Current biology : CB · 2021Article
- Identification of leukemia stem cell expression signatures through Monte Carlo feature selection strategy and support vector machine.Cancer gene therapy · 2020Article
- Substrate complex competition is a regulatory motif that allows NFκB RelA to license but not amplify NFκB RelB.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Multiple Mechanisms Inactivate the LIN-41 RNA-Binding Protein To Ensure a Robust Oocyte-to-Embryo Transition inGenetics · 2018Article
- Genome Stability during Cell Proliferation: A Systems Analysis of the Molecular Mechanisms Controlling Progression through the Eukaryotic Cell Cycle.Current opinion in systems biology · 2018Article
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
The cell division cycle is the process by which eukaryotic cells replicate their chromosomes and partition them to two daughter cells. To maintain the integrity of the genome, proliferating cells must be able to block progression through the division cycle at key transition points (called "checkpoints") if there have been problems in the replication of the chromosomes or their biorientation on the mitotic spindle. These checkpoints are governed by protein-interaction networks, composed of phase-specific cell-cycle activators and inhibitors. Examples include Cdk1:Clb5 and its inhibitor Sic1 at the G1/S checkpoint in budding yeast, APC:Cdc20 and its inhibitor MCC at the mitotic checkpoint, and PP2A:B55 and its inhibitor, alpha-endosulfine, at the mitotic-exit checkpoint. Each of these inhibitors is a substrate as well as a stoichiometric inhibitor of the cell-cycle activator. Because the production of each inhibitor is promoted by a regulatory protein that is itself inhibited by the cell-cycle activator, their interaction network presents a regulatory motif characteristic of a "feedback-amplified domineering substrate" (FADS). We describe how the FADS motif responds to signals in the manner of a bistable toggle switch, and then we discuss how this toggle switch accounts for the abrupt and irreversible nature of three specific cell-cycle checkpoints.
Indexed as
Identifiers
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.