ArticleNucleic acids research2008
Human abasic endonuclease action on multilesion abasic clusters: implications for radiation-induced biological damage.
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 33 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
33 citing papers in PubMed.
- Structural basis for the mechanism and stability of the EEPD1 5' endonuclease.The Journal of biological chemistry · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- Review
- EEPD1 promotes repair of oxidatively-stressed replication forks.NAR cancer · 2023Article
- A combinatorial system to examine the enzymatic repair of multiply damaged DNA substrates.Nucleic acids research · 2022Article
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
- Mutagenic Effects of a 2-Deoxyribonolactone-Thymine Glycol Tandem DNA Lesion in Human Cells.Biochemistry · 2020Article
- Expanded Substrate Scope of DNA Polymerase θ and DNA Polymerase β: Lyase Activity on 5'-Overhangs and Clustered Lesions.Biochemistry · 2018Article
- Scaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesions.Oncotarget · 2016Article
- Histone deacetylase inhibitors decrease NHEJ both by acetylation of repair factors and trapping of PARP1 at DNA double-strand breaks in chromatin.Leukemia research · 2016Article
- Accelerated processing of solitary and clustered abasic site DNA damage lesions by APE1 in the presence of aqueous extract of Ganoderma lucidum.Journal of biosciences · 2016Article
- Article
- Article
- Nucleotide excision repair of chemically stabilized analogues of DNA interstrand cross-links produced from oxidized abasic sites.Biochemistry · 2014Article
- Increased mutability and decreased repairability of a three-lesion clustered DNA-damaged site comprised of an AP site and bi-stranded 8-oxoG lesions.International journal of radiation biology · 2014Article
- APE1 incision activity at abasic sites in tandem repeat sequences.Journal of molecular biology · 2014Article
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- Clustered DNA lesions containing 5-formyluracil and AP site: repair via the BER system.PloS one · 2013Article
- DNA damage-induced primordial follicle oocyte apoptosis and loss of fertility require TAp63-mediated induction of Puma and Noxa.Molecular cell · 2012Article
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.
Funding
Abstract
Clustered damages-two or more closely opposed abasic sites, oxidized bases or strand breaks-are induced in DNA by ionizing radiation and by some radiomimetic drugs. They are potentially mutagenic or lethal. High complexity, multilesion clusters (three or more lesions) are hypothesized as repair-resistant and responsible for the greater biological damage induced by high linear energy transfer radiation (e.g. charged particles) than by low linear energy transfer X- or gamma-rays. We tested this hypothesis by assessing human abasic endonuclease Ape1 activity on two- and multiple-lesion abasic clusters. We constructed cluster-containing oligonucleotides using a central variable cassette with abasic site(s) at specific locations, and 5' and 3' terminal segments tagged with visually distinctive fluorophores. The results indicate that in two- or multiple-lesion clusters, the spatial arrangement of uni-sided positive [in which the opposing strand lesion(s) is 3' to the base opposite the reference lesion)] or negative polarity [opposing strand lesion(s) 5' to the base opposite the reference lesion] abasic clusters is key in determining Ape1 cleavage efficiency. However, no bipolar clusters (minimally three-lesions) were good Ape1 substrates. The data suggest an underlying molecular mechanism for the higher levels of biological damage associated with agents producing complex clusters: the induction of highly repair-resistant bipolar clusters.
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.