Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Integrated Stochastic Model of DNA Damage Repair by Non-homologous End Joining and p53/p21- Mediated Early Senescence Signalling

28 May 2015

Abstract excerpt

Unrepaired or inaccurately repaired DNA damage can lead to a range of cell fates, such as apoptosis, cellular senescence or cancer, depending on the efficiency and accuracy of DNA damage repair and on the downstream DNA damage signalling. DNA damage repair and signalling have been studied and modelled in detail separately, but it is not yet clear how they integrate with one another to control cell fate. In this...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA Repair Mechanisms
Share to PARP inhibition in cancer therapy
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26020242
DOI: 10.1371/journal.pcbi.1004246

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Integrated Stochastic Model of DNA Damage Repair by Non-homologous End Joining and p53/p21- Mediated Early Senescence SignallingPMID 26020242Read ↗

Modelling the onset of senescence at the G1/S cell cycle checkpoint.Semantic proximity Read ↗

Unrepairable DNA double-strand breaks that are generated by ionising radiation determine the fate of normal human cells.Semantic proximity Read ↗

Mechanistic Modelling of DNA Repair and Cellular Survival Following Radiation-Induced DNA Damage.Semantic proximity Read ↗

Both Complexity and Location of DNA Damage Contribute to Cellular Senescence Induced by Ionizing RadiationSemantic proximity Read ↗

Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescenceSemantic proximity Read ↗

Mechanistic modelling and Bayesian inference elucidates the variable dynamics of double-strand break repairSemantic proximity Read ↗

A stochastic model of cell replicative senescence based on telomere shortening, oxidative stress, and somatic mutations in nuclear and mitochondrial DNA.Semantic proximity Read ↗

Biphasic JNK–Erk Signaling Separates Induction and Maintenance of Cell Senescence after DNA DamageSemantic proximity Read ↗

The BIANCA model/code of radiation-induced cell death: application to human cells exposed to different radiation typesSemantic proximity Read ↗

The role of telomere shortening in carcinogenesis: A hybrid stochastic-deterministic approachSemantic proximity Read ↗

Biochemical Kinetics Model of DSB Repair and Induction of γ-H2AX Foci by Non-homologous End JoiningSemantic proximity Read ↗

A Kinetic-Based Model of Radiation-Induced Intercellular SignallingSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.