ArticleBMC genomics2014
Modelling the onset of senescence at the G1/S cell cycle checkpoint.
Article in BMC genomics, 2014. 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, 47 citations in OpenAlex.
- Ethyl acetate extract ofResearch in pharmaceutical sciences · 2026Article
- Synthetic lethality and DNA damage response targeting in cancer stem cells: a comprehensive review.Discover oncology · 2026Review
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Micro-RNA-140-3p Acts as a Tumor Suppressor Gene in Acute Promyelocytic Leukemia by Targeting Hepatocyte Growth Factor.Cell biochemistry and biophysics · 2025Article
- Mesenchymal stem cell-derived exosomal CBLB ameliorates infantile pneumonia progression probably by ubiquitinating MAPK14.Journal of inflammation (London, England) · 2025Article
- Ethanol extract fromNarra J · 2025Article
- A comprehensive review of computational cell cycle models in guiding cancer treatment strategies.NPJ systems biology and applications · 2024Review
- Reducing Boolean networks with backward equivalence.BMC bioinformatics · 2023Article
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- Synergistic effects of complex drug combinations in colorectal cancer cells predicted by logical modelling.Frontiers in systems biology · 2023Article
- LINCing Senescence and Nuclear Envelope Changes.Cells · 2022Review
- The Effects of Muscle Cell Aging on Myogenesis.International journal of molecular sciences · 2021Article
- Nickel carcinogenesis mechanism: cell cycle dysregulation.Environmental science and pollution research international · 2021Review
- TRIM27 Functions as a Novel Oncogene in Non-Triple-Negative Breast Cancer by Blocking Cellular Senescence through p21 Ubiquitination.Molecular therapy. Nucleic acids · 2020Article
- Systems biology approach suggests new miRNAs as phenotypic stability factors in the epithelial-mesenchymal transition.Journal of the Royal Society, Interface · 2020Article
- Article
- An inducible MAO-B mouse model of Parkinson's disease: a tool towards better understanding basic disease mechanisms and developing novel therapeutics.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Lycorine: A prospective natural lead for anticancer drug discovery.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018Review
- A Novel Data-Driven Boolean Model for Genetic Regulatory Networks.Frontiers in physiology · 2018Article
- Ponatinib promotes a G1 cell-cycle arrest of merlin/NF2-deficient human schwann cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDNA damage (single or double-strand breaks) triggers adapted cellular responses. These responses are elicited through signalling pathways, which activate cell cycle checkpoints and basically lead to three cellular fates: cycle arrest promoting DNA repair, senescence (permanent arrest) or cell death. Cellular senescence is known for having a tumour-suppressive function and its regulation arouses a growing scientific interest. Here, we advance a qualitative model covering DNA damage response pathways, focusing on G1/S checkpoint enforcement, supposedly more sensitive to arrest than G2/M checkpoint.
resultsWe define a discrete, logical model encompassing ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related) pathways activation upon DNA damage, as well as G1/S checkpoint main components. It also includes the stress responsive protein p38MAPK (mitogen-activated protein kinase 14) known to be involved in the regulation of senescence. The model has four outcomes that convey alternative cell fates: proliferation, (transient) cell cycle arrest, apoptosis and senescence. Different levels of DNA damage are considered, defined by distinct combinations of single and double-strand breaks. Each leads to a single stable state denoting the cell fate adopted upon this specific damage. A range of model perturbations corresponding to gene loss-of-function or gain-of-function is compared to experimental mutations.
conclusionsAs a step towards an integrative model of DNA-damage response pathways to better cover the onset of senescence, our model focuses on G1/S checkpoint enforcement. This model qualitatively agrees with most experimental observations, including experiments involving mutations. Furthermore, it provides some predictions.
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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.