ArticleNucleic acids research2008
Apn1 and Apn2 endonucleases prevent accumulation of repair-associated DNA breaks in budding yeast as revealed by direct chromosomal analysis.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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.
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Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Review
- Complex Mechanisms of Antimony Genotoxicity in Budding Yeast Involves Replication and Topoisomerase I-Associated DNA Lesions, Telomere Dysfunction and Inhibition of DNA Repair.International journal of molecular sciences · 2021Article
- Genetic Characterization of Three Distinct Mechanisms Supporting RNA-Driven DNA Repair and Modification Reveals Major Role of DNA Polymerase ζ.Molecular cell · 2020Article
- Mutation signatures specific to DNA alkylating agents in yeast and cancers.Nucleic acids research · 2020Article
- Genomic alterations and abnormal expression of APE2 in multiple cancers.Scientific reports · 2020Article
- Systematic analysis of linker histone PTM hotspots reveals phosphorylation sites that modulate homologous recombination and DSB repair.DNA repair · 2020Article
- Molecular signatures of aneuploidy-driven adaptive evolution.Nature communications · 2020Article
- Studying DNA Double-Strand Break Repair: An Ever-Growing Toolbox.Frontiers in molecular biosciences · 2020Review
- Global Analysis of Furfural-Induced Genomic Instability Using a Yeast Model.Applied and environmental microbiology · 2019Article
- Bacterial Ligase D preternary-precatalytic complex performs efficient abasic sites processing at double strand breaks during nonhomologous end joining.Nucleic acids research · 2019Article
- Genome-wide analysis of genomic alterations induced by oxidative DNA damage in yeast.Nucleic acids research · 2019Article
- Article
- Increased chromosomal mobility after DNA damage is controlled by interactions between the recombination machinery and the checkpoint.Genes & development · 2018Article
- Flap endonuclease overexpression drives genome instability and DNA damage hypersensitivity in a PCNA-dependent manner.Nucleic acids research · 2018Article
- i-BLESS is an ultra-sensitive method for detection of DNA double-strand breaks.Communications biology · 2018Article
- Multi-scale tracking reveals scale-dependent chromatin dynamics after DNA damage.Molecular biology of the cell · 2017Article
- Replication fork slowing and stalling are distinct, checkpoint-independent consequences of replicating damaged DNA.PLoS genetics · 2017Article
- APOBEC3B cytidine deaminase targets the non-transcribed strand of tRNA genes in yeast.DNA repair · 2017Article
- Mechanisms of glycosylase induced genomic instability.PloS one · 2017Article
- The Shu complex promotes error-free tolerance of alkylation-induced base excision repair products.Nucleic acids research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Base excision repair (BER) provides relief from many DNA lesions. While BER enzymes have been characterized biochemically, BER functions within cells are much less understood, in part because replication bypass and double-strand break (DSB) repair can also impact resistance to base damage. To investigate BER in vivo, we examined the repair of methyl methanesulfonate (MMS) induced DNA damage in haploid G1 yeast cells, so that replication bypass and recombinational DSB repair cannot occur. Based on the heat-lability of MMS-induced base damage, an assay was developed that monitors secondary breaks in full-length yeast chromosomes where closely spaced breaks yield DSBs that are observed by pulsed-field gel electrophoresis. The assay detects damaged bases and abasic (AP) sites as heat-dependent breaks as well as intermediate heat-independent breaks that arise during BER. Using a circular chromosome, lesion frequency and repair kinetics could be easily determined. Monitoring BER in single and multiple glycosylase and AP-endonuclease mutants confirmed that Mag1 is the major enzyme that removes MMS-damaged bases. This approach provided direct physical evidence that Apn1 and Apn2 not only repair cellular base damage but also prevent break accumulation that can result from AP sites being channeled into other BER pathway(s).
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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.