ReviewCurrent molecular pharmacology2012
Overview of base excision repair biochemistry.
Review in Current molecular pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 2 of them syntheses that pooled it.
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
165 citing papers in PubMed, 2 syntheses or guidelines pooled it, 299 citations in OpenAlex.
- Research progress on the role and mechanism of DNA damage repair in germ cell development.Frontiers in endocrinology · 2023Pooled it
- Association between the 8-oxoguanine DNA glycosylase gene Ser326Cys polymorphism and age-related cataract: a systematic review and meta-analysis.International ophthalmology · 2018Pooled it
- DNA damage induces long range changes to duplex structure-a non-protein start to damage detection?Nucleic acids research · 2026Article
- Molecular basis of nick ligation in the nucleosome by DNA Ligase IIIα.Nature communications · 2026Article
- DNA damage at an early developmental stage affects neurodevelopment in sterlet (Acipenser ruthenus).BMC biology · 2026Article
- Structural basis for uracil removal from DNA by human SMUG1.Nature communications · 2026Article
- Single-Nucleotide Polymorphisms in Genes Associated with Mitochondrial and DNA Damage Response Modulate the Risk of Non-Alcoholic Fatty Liver Disease in Humans.International journal of molecular sciences · 2026Article
- The essential role of hydrogen gas recycling by gut microbes in reducing deuterium load in host mitochondria: is trimethylamine oxide a deuterium sensor?Metabolomics : Official journal of the Metabolomic Society · 2026Review
- Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancer.Research square · 2025Article
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- CHCHD4 Oxidoreductase Activity: A Comprehensive Analysis of the Molecular, Functional, and Structural Properties of Its Redox-Regulated Substrates.Molecules (Basel, Switzerland) · 2025Review
- Advancements in Osteosarcoma Therapy: Overcoming Chemotherapy Resistance and Exploring Novel Pharmacological Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Repair pathway coordination from gap filling by polβ and subsequent nick sealing by LIG1 or LIG3α governs BER efficiency at the downstream steps.DNA repair · 2025Article
- DNA repair and disease: insights from the human DNA glycosylase NEIL family.Experimental & molecular medicine · 2025Review
- Cancer prognosis using base excision repair genes.Molecules and cells · 2025Review
- Structural and Functional Insights into UDGs.Protein and peptide letters · 2025Review
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- An Insight into the Mechanism of DNA Cleavage by DNA Endonuclease from the Hyperthermophilic ArchaeonInternational journal of molecular sciences · 2024Article
- DNA Repair Protein XRCC1 Stimulates Activity of DNA Polymerase λ under Conditions of Microphase Separation.International journal of molecular sciences · 2024Article
105 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Base excision repair (BER) is an evolutionarily conserved pathway, which could be considered the "workhorse" repair mechanism of the cell. In particular, BER corrects most forms of spontaneous hydrolytic decay products in DNA, as well as everyday oxidative and alkylative modifications to bases or the sugar phosphate backbone. The repair response involves five key enzymatic steps that aim to remove the initial DNA lesion and restore the genetic material back to its original state: (i) excision of a damaged or inappropriate base, (ii) incision of the phosphodiester backbone at the resulting abasic site, (iii) termini clean-up to permit unabated repair synthesis and/or nick ligation, (iv) gap-filling to replace the excised nucleotide, and (v) sealing of the final, remaining DNA nick. These repair steps are executed by a collection of enzymes that include DNA glycosylases, apurinic/apyrimidinic endonucleases, phosphatases, phosphodiesterases, kinases, polymerases and ligases. Defects in BER components lead to reduced cell survival, elevated mutation rates, and DNA-damaging agent hypersensitivities. In addition, the pathway plays a significant role in determining cellular responsiveness to relevant clinical anti-cancer agents, such as alkylators (e.g. temozolomide), nucleoside analogs (e.g. 5-fluorouracil), and ionizing radiation. The molecular details of BER and the contribution of the pathway to therapeutic agent resistance are reviewed herein.
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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.