ArticleMutation research2009
Cells deficient in PARP-1 show an accelerated accumulation of DNA single strand breaks, but not AP sites, over the PARP-1-proficient cells exposed to MMS.
Article in Mutation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Suppression of isoprenylcysteine carboxylmethyltransferase compromises DNA damage repair.Life science alliance · 2021Article
- Review
- In silico screening identifies a novel small molecule inhibitor that counteracts PARP inhibitor resistance in ovarian cancer.Scientific reports · 2021Article
- Review
- PARP Inhibitors: Clinical Relevance, Mechanisms of Action and Tumor Resistance.Frontiers in cell and developmental biology · 2020Review
- Targeting Base Excision Repair in Cancer: NQO1-Bioactivatable Drugs Improve Tumor Selectivity and Reduce Treatment Toxicity Through Radiosensitization of Human Cancer.Frontiers in oncology · 2020Review
- MacroH2A1 Regulation of Poly(ADP-Ribose) Synthesis and Stability Prevents Necrosis and Promotes DNA Repair.Molecular and cellular biology · 2019Article
- Article
- The multifaceted roles of PARP1 in DNA repair and chromatin remodelling.Nature reviews. Molecular cell biology · 2017Review
- ALC1/CHD1L, a chromatin-remodeling enzyme, is required for efficient base excision repair.PloS one · 2017Article
- Suicidal cross-linking of PARP-1 to AP site intermediates in cells undergoing base excision repair.Nucleic acids research · 2014Article
- Incidence and prognostic value of multiple gene promoter methylations in gliomas.Journal of neuro-oncology · 2014Article
- Repair of DNA strand breaks in a minichromosome in vivo: kinetics, modeling, and effects of inhibitors.PloS one · 2013Article
- Hyperactivation of PARP triggers nonhomologous end-joining in repair-deficient mouse fibroblasts.PloS one · 2012Article
- Damage-induced localized hypermutability.Cell cycle (Georgetown, Tex.) · 2011Article
- Classifying DNA repair genes by kernel-based support vector machines.Bioinformation · 2011Article
- Apurinic/apyrimidinic (AP) site recognition by the 5'-dRP/AP lyase in poly(ADP-ribose) polymerase-1 (PARP-1).Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Accumulation of true single strand breaks and AP sites in base excision repair deficient cells.Mutation research · 2010Article
- Alkylation DNA damage in combination with PARP inhibition results in formation of S-phase-dependent double-strand breaks.DNA repair · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) is a base excision repair (BER) protein that binds to DNA single strand breaks (SSBs) and subsequently synthesizes and transfers poly(ADP-ribose) polymers to various nuclear proteins. Numerous biochemical studies have implicated PARP-1 as a modulator of BER; however, the role of PARP-1 in BER in living cells remains unclear partly due to lack of accurate quantitation of BER intermediates existing in cells. Since DT40 cells, chicken B lymphocytes, naturally lack PARP-2, DT40 cells allow for the investigation of the PARP-1 null phenotype without confounding by PARP-2. To test the hypothesis that PARP-1 is necessary for efficient BER during methylmethane sulfonate (MMS) exposure in vertebrate cells, intact DT40 cells and their isogenic PARP-1 null counterparts were challenged with different exposure scenarios for phenotypic characterization. With chronic exposure, PARP-1 null cells exhibited sensitivity to MMS but with an acute exposure did not accumulate base lesions or AP sites to a greater extent than wild-type cells. However, an increase in SSB content in PARP-1 null cell DNA, as indicated by glyoxal gel electrophoresis under neutral conditions, suggested the presence of BER intermediates. These data suggest that during exposure, PARP-1 impacts the stage of BER after excision of the deoxyribosephosphate moiety from the 5' end of DNA strand breaks by polymerase beta.
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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.