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

p53 mediates senescence-like arrest induced by chronic replicational stress.

Molecular and cellular biology - 1 Aug 2007

Marusyk Andriy, Wheeler Linda J, Mathews Christopher K, DeGregori James

Abstract excerpt

Previous studies have shown that exposure of cells to high levels of replicational stress leads to permanent proliferation arrest that does not require p53. We have examined cellular responses to therapeutically relevant low levels of replicational stress that allow limited proliferation. Chronic...

Read the complete abstract on PubMed

Topics

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

Share to Aphidicolin
Share to Cellular Senescence
Share to Checkpoint Kinase 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Cyclin-Dependent Kinase Inhibitor p21

Share to Herpes Simplex Virus Protein Vmw65

Share to Nucleotides

Share to Rad51 Recombinase

Source

Open in PubMed Open full text

Identifiers

PMID: 17515610
DOI: 10.1128/MCB.01316-06
PMCID: PMC1952086

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17515610-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

p53 mediates senescence-like arrest induced by chronic replicational stress.PMID 17515610Read ↗

Replicational stress selects for p53 mutation.Semantic proximity Read ↗

Chk1 and p21 Cooperate to Prevent Apoptosis during DNA Replication Fork StressSemantic proximity Read ↗

Significance of Wild-Type p53 Signaling in Suppressing Apoptosis in Response to Chemical Genotoxic Agents: Impact on Chemotherapy OutcomeSemantic proximity Read ↗

Tumour suppressors, kinases and clamps: How p53 regulates the cell cycle in response to DNA damageSemantic proximity Read ↗

Persistent DNA damage caused by low levels of mitomycin C induces irreversible cell senescenceSemantic proximity Read ↗

Effects of p21 <sup>Waf1/Cip1/Sdi1</sup> on cellular gene expression: Implications for carcinogenesis, senescence, and age-related diseasesSemantic proximity Read ↗

Common Chemical Inductors of Replication Stress: Focus on Cell‐Based StudiesSemantic proximity Read ↗

Overexpression of Cyclin E1 or Cdc25A leads to replication stress, mitotic aberrancies, and increased sensitivity to replication checkpoint inhibitorsSemantic proximity Read ↗

Loss of proliferative capacity and induction of senescence in oxidatively stressed human fibroblasts.Semantic proximity Read ↗

New insights into p53 signaling and cancer cell response to DNA damage: implications for cancer therapy.Semantic proximity Read ↗

Rapamycin decelerates cellular senescenceSemantic proximity Read ↗

Replication stress triggers microsatellite destabilization and hypermutation leading to clonal expansion in vitroSemantic proximity Read ↗

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