ArticleOncogene2002
Implication of p53 in base excision DNA repair: in vivo evidence.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 114 citations in OpenAlex.
- The OGG1 Ser326Cys polymorphism: molecular mechanisms of disease susceptibility and precision medicine applications.Clinical epigenetics · 2025Review
- Novel Expression of Thymine Dimers in Renal Cell Carcinoma, Demonstrated through Immunohistochemistry.Biomedicines · 2022Article
- Huwe1 supports B-cell development, B-cell-dependent immunity, somatic hypermutation and class switch recombination by regulating proliferation.Frontiers in immunology · 2022Article
- Review
- A Modern Genotoxicity Testing Paradigm: Integration of the High-Throughput CometChip® and the TGx-DDI Transcriptomic Biomarker in Human HepaRG™ Cell Cultures.Frontiers in public health · 2021Article
- Do Mutations Turn p53 into an Oncogene?International journal of molecular sciences · 2019Review
- Exploring the Antioxidant Effects and Periodic Regulation of Cancer Cells by Polyphenols Produced by the Fermentation of Grape Skin by Lactobacillus plantarum KFY02.Biomolecules · 2019Article
- Effect of the Interaction Between Selenium and Zinc on DNA Repair in Association With Cancer Prevention.Journal of cancer prevention · 2019Review
- Tissue specificity of DNA damage response and tumorigenesis.Cancer biology & medicine · 2019Article
- p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells.PloS one · 2017Article
- Article
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- Facilitation of base excision repair by chromatin remodeling.DNA repair · 2015Review
- Mitotic UV irradiation induces a DNA replication-licensing defect that potentiates G1 arrest response.PloS one · 2015Article
- Unravelling mechanisms of p53-mediated tumour suppression.Nature reviews. Cancer · 2014Article
- The significance of the alteration of 8-OHdG in serous ovarian carcinoma.Journal of ovarian research · 2013Article
- DNA damage in human pterygium: one-shot multiple targets.Molecular vision · 2013Article
- Transcriptional regulation of thymine DNA glycosylase (TDG) by the tumor suppressor protein p53.Cell cycle (Georgetown, Tex.) · 2012Article
- Pol β associated complex and base excision repair factors in mouse fibroblasts.Nucleic acids research · 2012Article
- The pattern of somatic hypermutation of Ig genes is altered when p53 is inactivated.Molecular immunology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 plays an important role in response to DNA damage, including DNA repair. One DNA repair pathway, nucleotide excision repair (NER), has been well-documented to be regulated by p53. It seemed probable that p53 may affect other DNA repair pathways. We employed matched isogenic pairs of cell lines, wild-type or p53-deficient, to investigate this question using methyl methanesulfonate (MMS), a base-damaging agent. Alkylation damage induced by MMS is repaired exclusively by the base excision repair (BER) pathway. Cells carrying mutant or no p53 genes exhibited slow BER of MMS-induced DNA damage, and exhibited MMS-sensitivity. One contributing factor is the abundance of DNA polymerase beta (beta-pol), an enzyme required for BER, which was almost absent in p53 mutant and p53-null cells. Our findings demonstrate an in vivo requirement for p53 in regulating the base excision repair response, a novel finding of great potential importance in understanding the DNA repair branch of the p53 pathway.
Indexed as
Identifiers
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.