ArticleNucleic acids research2023
Mechanistic insight into AP-endonuclease 1 cleavage of abasic sites at stalled replication fork mimics.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- XRCC1 deficiency drives telomeric chromatin leakage, inflammatory signalling and senescence.Redox biology · 2026Article
- Computation and Structure-Guided Arginine Scanning Engineers a Hyperactive AP Endonuclease for Multiplex Viral RNA Sensing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A dynamic search mechanism enables APE1 to identify AP-sites in DNA.Nucleic acids research · 2026Article
- APE1 coordinates its disordered region and metal cofactors to drive genome surveillance.Nucleic acids research · 2026Article
- UNG-RPA interaction governs the choice between high-fidelity and mutagenic uracil repair.Nucleic acids research · 2026Article
- APE1 Activity is Controlled by Non-G-Quadruplex Conformations in Single- and Double-Stranded G-Quadruplex Constructs.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Genome-wide maps of CPD deamination in yeast reveal the impact of DNA sequence context and nucleosome architecture on cytosine deamination rates.Genome research · 2026Article
- PCNA encircling primer/template junctions is eliminated by exchange of RPA for Rad51: implications for the interplay between human DNA damage tolerance pathways.Nucleic acids research · 2026Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- Divergent evolution of opposite base specificity and single-stranded DNA activity in animal and plant AP endonucleases.Nucleic acids research · 2025Article
- Review
- Partial wrapping of single-stranded DNA by replication protein A and modulation through phosphorylation.Nucleic acids research · 2024Article
- Endogenous base damage as a driver of genomic instability in homologous recombination-deficient cancers.DNA repair · 2024Review
- Replication protein A dynamically re-organizes on primer/template junctions to permit DNA polymerase δ holoenzyme assembly and initiation of DNA synthesis.Nucleic acids research · 2024Article
- Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024Article
- Direct, ensemble FRET approaches to monitor transient state kinetics of human DNA polymerase δ holoenzyme assembly and initiation of DNA synthesis.Methods in enzymology · 2024Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Many types of damage, including abasic sites, block replicative DNA polymerases causing replication fork uncoupling and generating ssDNA. AP-Endonuclease 1 (APE1) has been shown to cleave abasic sites in ssDNA. Importantly, APE1 cleavage of ssDNA at a replication fork has significant biological implications by generating double strand breaks that could collapse the replication fork. Despite this, the molecular basis and efficiency of APE1 processing abasic sites at replication forks remain elusive. Here, we investigate APE1 cleavage of abasic substrates that mimic APE1 interactions at stalled replication forks or gaps. We determine that APE1 has robust activity on these substrates, like dsDNA, and report rates for cleavage and product release. X-ray structures visualize the APE1 active site, highlighting an analogous mechanism is used to process ssDNA substrates as canonical APE1 activity on dsDNA. However, mutational analysis reveals R177 to be uniquely critical for the APE1 ssDNA cleavage mechanism. Additionally, we investigate the interplay between APE1 and Replication Protein A (RPA), the major ssDNA-binding protein at replication forks, revealing that APE1 can cleave an abasic site while RPA is still bound to the DNA. Together, this work provides molecular level insights into abasic ssDNA processing by APE1, including the presence of RPA.
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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.