ArticleNucleic acids research2019
Nucleotide excision repair of abasic DNA lesions.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Assessment and detection of nucleotide excision repair capability in human cells: a critical review of current functional methods.Molecular biology reports · 2026Review
- Abasic site repair in APE1-deficient mouse embryonic stem cells: a matter for the MRN complex and ATM signaling.Nucleic acids research · 2026Article
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2026Article
- Article
- Synthesis of functionalized, 13-alkyl-substituted coralyne derivatives and investigation of their interactions with duplex and abasic site-containing DNA.Beilstein journal of organic chemistry · 2026Article
- Structural snapshots of the mechanism of ATP-dependent DNA damage recognition by UvrA.Nature communications · 2025Article
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Transcription blocking properties and transcription-coupled repair of NThe Journal of biological chemistry · 2025Article
- CHD6 has poly(ADP-ribose)- and DNA-binding domains and regulates PARP1/2-trapping inhibitor sensitivity via abasic site repair.Nature communications · 2025Article
- Exploring the Potential of Malvidin and Echiodinin as Probable Antileishmanial Agents Through In Silico Analysis and In Vitro Efficacy.Molecules (Basel, Switzerland) · 2025Article
- Targeted Drug Nanodelivery and Immunotherapy for Combating Tumor Resistance.Combinatorial chemistry & high throughput screening · 2025Review
- Repair and DNA Polymerase Bypass of Clickable Pyrimidine Nucleotides.Biomolecules · 2024Article
- Probing the Conformational Restraints of DNA Damage Recognition with β-L-Nucleotides.International journal of molecular sciences · 2024Article
- Back-Up Base Excision DNA Repair in Human Cells Deficient in the Major AP Endonuclease, APE1.International journal of molecular sciences · 2023Article
- Unprecedented reactivity of polyamines with aldehydic DNA modifications: structural determinants of reactivity, characterization and enzymatic stability of adducts.Nucleic acids research · 2023Article
- APEX1 Nuclease and Redox Functions are Both Essential for Adult Mouse Hematopoietic Stem and Progenitor Cells.Stem cell reviews and reports · 2023Article
- Requirement of transcription-coupled nucleotide excision repair for the removal of a specific type of oxidatively induced DNA damage.Nucleic acids research · 2023Article
- Recognition of a Clickable Abasic Site Analog by DNA Polymerases and DNA Repair Enzymes.International journal of molecular sciences · 2022Article
- Transcriptional Perturbations of 2,6-Diaminopurine and 2-Aminopurine.ACS chemical biology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, we demonstrate that nucleotide excision repair pathway (NER) efficiently removes BER-resistant AP lesions and significantly enhances the repair of APE1-sensitive ones. Our results further indicate that core NER components XPA and XPF are equally required and that both global genome (GG-NER) and transcription coupled (TC-NER) subpathways contribute to the repair.
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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.