ArticleThe EMBO journal2001
A role for p53 in base excision repair.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
108 citing papers in PubMed, 327 citations in OpenAlex.
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- Targeting APE1: Advancements in the Diagnosis and Treatment of Tumors.Protein and peptide letters · 2025Review
- The BCL11A transcription factor stimulates the enzymatic activities of the OGG1 DNA glycosylase.Biological chemistry · 2024Article
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- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.Nucleic acids research · 2024Article
- The DNA repair function of BCL11A suppresses senescence and promotes continued proliferation of triple-negative breast cancer cells.NAR cancer · 2022Article
- Delineating functional mechanisms of the p53/p63/p73 family of transcription factors through identification of protein-protein interactions using interface mimicry.Molecular carcinogenesis · 2022Article
- Review
- Base excision repair accessory factors in senescence avoidance and resistance to treatments.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Impact of the interplay between stemness features, p53 and pol iota on replication pathway choices.Nucleic acids research · 2021Article
- Selective therapeutic strategy for p53-deficient cancer by targeting dysregulation in DNA repair.Communications biology · 2021Article
- CUT Domain Proteins in DNA Repair and Cancer.Cancers · 2021Review
- Article
- Review
- p53 is required for nuclear but not mitochondrial DNA damage-induced degeneration.Cell death & disease · 2021Article
- Role of Dietary Antioxidants in p53-Mediated Cancer Chemoprevention and Tumor Suppression.Oxidative medicine and cellular longevity · 2021Review
- Multiple biochemical properties of the p53 molecule contribute to activation of polymerase iota-dependent DNA damage tolerance.Nucleic acids research · 2020Article
- Moonlighting Proteins in the Fuzzy Logic of Cellular Metabolism.Molecules (Basel, Switzerland) · 2020Review
- p53 Disruption Increases Uracil Accumulation in DNA of Murine Embryonic Fibroblasts and Leads to Folic Acid-Nonresponsive Neural Tube Defects in Mice.The Journal of nutrition · 2020Article
48 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
Wild-type p53 protein can markedly stimulate base excision repair (BER) in vitro, either reconstituted with purified components or in extracts of cells. In contrast, p53 with missense mutations either at hot-spots in the core domain or within the N-terminal transactivation domain is defective in this function. Stimulation of BER by p53 is correlated with its ability to interact directly both with the AP endonuclease (APE) and with DNA polymerase beta (pol beta). Furthermore, p53 stabilizes the interaction between DNA pol beta and abasic DNA. Evidence that this function of p53 is physiologically relevant is supported by the facts that BER activity in human and murine cell extracts closely parallels their levels of endogenous p53, and that BER activity is much reduced in cell extracts immunodepleted of p53. These data suggest a novel role for p53 in DNA repair, which could contribute to its function as a key tumor suppressor.
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What OpenQuestion holds
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.