ArticleNature2014
Aprataxin resolves adenylated RNA-DNA junctions to maintain genome integrity.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 110 citations in OpenAlex.
- Fidelity of DNA ligase I is sensitive to physiological MgThe Journal of biological chemistry · 2026Article
- Stable Hypermutators Revealed by the Genomic Landscape of Genes Involved in Genome Stability Among Yeast Species.Molecular biology and evolution · 2025Article
- Induced pluripotent stem cells carrying novel APTX mutations presented defective neural differentiation with the accumulation of DNA single-strand breaks.Cell death discovery · 2025Article
- Molecular basis for RNA discrimination by human DNA ligase 1.Nucleic acids research · 2025Article
- Discovery of reversing enzymes for RNA ADP-ribosylation reveals a possible defence module against toxic attack.Nucleic acids research · 2025Article
- Regulation of endocrine cell alternative splicing revealed by single-cell RNA sequencing in type 2 diabetes pathogenesis.Communications biology · 2024Article
- Processing of matched and mismatched rNMPs in DNA by archaeal ribonucleotide excision repair.iScience · 2023Article
- Mechanistic insight into AP-endonuclease 1 cleavage of abasic sites at stalled replication fork mimics.Nucleic acids research · 2023Article
- APTX acts in DNA double-strand break repair in a manner distinct from XRCC4.Journal of radiation research · 2023Article
- Flap endonuclease Rad27 cleaves the RNA of R-loop structures to suppress telomere recombination.Nucleic acids research · 2023Article
- The DNA repair enzyme, aprataxin, plays a role in innate immune signaling.Frontiers in aging neuroscience · 2023Article
- Molecular basis for processing of topoisomerase 1-triggered DNA damage by Apn2/APE2.Cell reports · 2022Article
- Ribonucleotide Incorporation by Eukaryotic B-Family Replicases and Its Implications for Genome Stability.Annual review of biochemistry · 2022Review
- Case report: A novelFrontiers in neurology · 2022Article
- Evaluation of repair activity by quantification of ribonucleotides in the genome.Genes to cells : devoted to molecular & cellular mechanisms · 2021Article
- LIG1 syndrome mutations remodel a cooperative network of ligand binding interactions to compromise ligation efficiency.Nucleic acids research · 2021Article
- Altered APE1 activity on abasic ribonucleotides is mediated by changes in the nucleoside sugar pucker.Computational and structural biotechnology journal · 2021Article
- High density of unrepaired genomic ribonucleotides leads to Topoisomerase 1-mediated severe growth defects in absence of ribonucleotide reductase.Nucleic acids research · 2020Article
- Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair.The EMBO journal · 2020Review
- Ligand binding characteristics of the Ku80 von Willebrand domain.DNA repair · 2020Article
3 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Faithful maintenance and propagation of eukaryotic genomes is ensured by three-step DNA ligation reactions used by ATP-dependent DNA ligases. Paradoxically, when DNA ligases encounter nicked DNA structures with abnormal DNA termini, DNA ligase catalytic activity can generate and/or exacerbate DNA damage through abortive ligation that produces chemically adducted, toxic 5'-adenylated (5'-AMP) DNA lesions. Aprataxin (APTX) reverses DNA adenylation but the context for deadenylation repair is unclear. Here we examine the importance of APTX to RNase-H2-dependent excision repair (RER) of a lesion that is very frequently introduced into DNA, a ribonucleotide. We show that ligases generate adenylated 5' ends containing a ribose characteristic of RNase H2 incision. APTX efficiently repairs adenylated RNA-DNA, and acting in an RNA-DNA damage response (RDDR), promotes cellular survival and prevents S-phase checkpoint activation in budding yeast undergoing RER. Structure-function studies of human APTX-RNA-DNA-AMP-Zn complexes define a mechanism for detecting and reversing adenylation at RNA-DNA junctions. This involves A-form RNA binding, proper protein folding and conformational changes, all of which are affected by heritable APTX mutations in ataxia with oculomotor apraxia 1. Together, these results indicate that accumulation of adenylated RNA-DNA may contribute to neurological disease.
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.