ArticleNucleic acids research2016
p53 coordinates base excision repair to prevent genomic instability.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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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.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Multi-omics analysis reveals the role of the XRCC gene family in diagnosis, prognosis, and immunity in pan-cancer.Discover oncology · 2026Article
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- Targeting the DNA damage response in cancer.MedComm · 2024Review
- Crosstalk between BER and NHEJ in XRCC4-Deficient Cells Depending on hTERT Overexpression.International journal of molecular sciences · 2024Article
- Genetics of ischemic stroke functional outcome.Journal of neurology · 2024Review
- Key Proteins of Replication Stress Response and Cell Cycle Control as Cancer Therapy Targets.International journal of molecular sciences · 2024Review
- The NUCKS1-SKP2-p21/p27 axis controls S phase entry.Nature communications · 2021Article
- Review
- Expression and prognostic analyses of the insulin-like growth factor 2 mRNA binding protein family in human pancreatic cancer.BMC cancer · 2020Article
- Review
- Resolving DNA Damage: Epigenetic Regulation of DNA Repair.Molecules (Basel, Switzerland) · 2020Review
- Persistent DNA damage triggers activation of the integrated stress response to promote cell survival under nutrient restriction.BMC biology · 2020Article
- The splicing component ISY1 regulates APE1 in base excision repair.DNA repair · 2020Article
- DNA repair in cancer initiation, progression, and therapy-a double-edged sword.Journal of applied genetics · 2019Review
- Inhibition of APE1-endonuclease activity affects cell metabolism in colon cancer cells via a p53-dependent pathway.DNA repair · 2019Article
- Transcription, Processing, and Decay of Mitochondrial RNA in Health and Disease.International journal of molecular sciences · 2019Review
- Dual Role of Nitric Oxide in Regulating the Response of β Cells to DNA Damage.Antioxidants & redox signaling · 2018Review
- Interplay between base excision repair protein XRCC1 and ALDH2 predicts overall survival in lung and liver cancer patients.Cellular oncology (Dordrecht, Netherlands) · 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
DNA constantly undergoes chemical modification due to endogenous and exogenous mutagens. The DNA base excision repair (BER) pathway is the frontline mechanism handling the majority of these lesions, and primarily involves a DNA incision and subsequent resealing step. It is imperative that these processes are extremely well-coordinated as unrepaired DNA single strand breaks (SSBs) can be converted to DNA double strand breaks during replication thus triggering genomic instability. However, the mechanism(s) governing the BER process are poorly understood. Here we show that accumulation of unrepaired SSBs triggers a p53/Sp1-dependent downregulation of APE1, the endonuclease responsible for the DNA incision during BER. Importantly, we demonstrate that impaired p53 function, a characteristic of many cancers, leads to a failure of the BER coordination mechanism, overexpression of APE1, accumulation of DNA strand breaks and results in genomic instability. Our data provide evidence for a previously unrecognized mechanism for coordination of BER by p53, and its dysfunction in p53-inactivated cells.
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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.