ArticleFrontiers in physiology2012
From quiescence to proliferation: Cdk oscillations drive the mammalian cell cycle.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Starve-Feed Cycles Direct Quiescence to Proliferation Transitions inbioRxiv : the preprint server for biology · 2026Article
- Cell Population Dynamics Informed by Cell-Cycle Regulation: A Deterministic Modeling Toolkit.Computational and structural biotechnology journal · 2026Review
- Inertial effect of cell state velocity on the quiescence-proliferation fate decision.NPJ systems biology and applications · 2024Article
- Cell state-directed therapy - epigenetic modulation of gene transcription demonstrated with a quantitative systems pharmacology model of temozolomide.CPT: pharmacometrics & systems pharmacology · 2023Article
- Target Mechanisms of the Cyanotoxin Cylindrospermopsin in Immortalized Human Airway Epithelial Cells.Toxins · 2022Article
- The Cardiac Sarcomere and Cell Cycle.Current cardiology reports · 2022Review
- Regulated interaction of ID2 with the anaphase-promoting complex links progression through mitosis with reactivation of cell-type-specific transcription.Nature communications · 2022Article
- Cyclin/Forkhead-mediated coordination of cyclin waves: an autonomous oscillator rationalizing the quantitative model of Cdk control for budding yeast.NPJ systems biology and applications · 2021Review
- The shifting shape and functional specializations of the cell cycle during lineage development.WIREs mechanisms of disease · 2021Review
- Trajectory-based energy landscapes of gene regulatory networks.Biophysical journal · 2021Article
- Clb3-centered regulations are recurrent across distinct parameter regions in minimal autonomous cell cycle oscillator designs.NPJ systems biology and applications · 2020Article
- Network mechanisms and dysfunction within an integrated computational model of progression through mitosis in the human cell cycle.PLoS computational biology · 2020Article
- Boolean model of anchorage dependence and contact inhibition points to coordinated inhibition but semi-independent induction of proliferation and migration.Computational and structural biotechnology journal · 2020Article
- Tox4 modulates cell fate reprogramming.Journal of cell science · 2019Article
- Robust synchronization of the cell cycle and the circadian clock through bidirectional coupling.Journal of the Royal Society, Interface · 2019Article
- Modeling the Dynamics of Let-7-Coupled Gene Regulatory Networks Linking Cell Proliferation to Malignant Transformation.Frontiers in physiology · 2019Article
- Coarse-graining and hybrid methods for efficient simulation of stochastic multi-scale models of tumour growth.Journal of computational physics · 2017Article
- Methylation ofOncology letters · 2017Article
- Principles of dynamical modularity in biological regulatory networks.Scientific reports · 2016Article
- The effects of intrinsic noise on the behaviour of bistable cell regulatory systems under quasi-steady state conditions.The Journal of chemical physics · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently proposed a detailed model describing the dynamics of the network of cyclin-dependent kinases (Cdks) driving the mammalian cell cycle (Gérard and Goldbeter, 2009). The model contains four modules, each centered around one cyclin/Cdk complex. Cyclin D/Cdk4-6 and cyclin E/Cdk2 promote progression in G1 and elicit the G1/S transition, respectively; cyclin A/Cdk2 ensures progression in S and the transition S/G2, while the activity of cyclin B/Cdk1 brings about the G2/M transition. This model shows that in the presence of sufficient amounts of growth factor the Cdk network is capable of temporal self-organization in the form of sustained oscillations, which correspond to the ordered, sequential activation of the various cyclin/Cdk complexes that control the successive phases of the cell cycle. The results suggest that the switch from cellular quiescence to cell proliferation corresponds to the transition from a stable steady state to sustained oscillations in the Cdk network. The transition depends on a finely tuned balance between factors that promote or hinder progression in the cell cycle. We show that the transition from quiescence to proliferation can occur in multiple ways that alter this balance. By resorting to bifurcation diagrams, we analyze the mechanism of oscillations in the Cdk network. Finally, we show that the complexity of the detailed model can be greatly reduced, without losing its key dynamical properties, by considering a skeleton model for the Cdk network. Using such a skeleton model for the mammalian cell cycle we show that positive feedback (PF) loops enhance the amplitude and the robustness of Cdk oscillations with respect to molecular noise. We compare the relative merits of the detailed and skeleton versions of the model for the Cdk network driving the mammalian cell cycle.
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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.