ArticleOncogene2005
Parp-1 deficiency causes an increase of deletion mutations and insertions/rearrangements in vivo after treatment with an alkylating agent.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 63 citations in OpenAlex.
- PARP-1 prevents osteoarthritis pathogenesis by inhibiting apoptosis in chondrocytes: an animal study.Arthritis research & therapy · 2026Article
- Tipping the PARylation scale: Dysregulation of PAR signaling in Huntington and neurodegenerative diseases.Journal of Huntington's disease · 2025Review
- DNA Alkylation Damage by Nitrosamines and Relevant DNA Repair Pathways.International journal of molecular sciences · 2023Review
- Existing Evidence for the Repurposing of PARP-1 Inhibitors in Rare Demyelinating Diseases.Cancers · 2022Review
- Functional roles of ADP-ribosylation writers, readers and erasers.Frontiers in cell and developmental biology · 2022Review
- DNA alkylation lesion repair: outcomes and implications in cancer chemotherapy.Journal of Zhejiang University. Science. B · 2021Review
- Modulation ofChemical research in toxicology · 2020Article
- Inflammation-induced DNA damage, mutations and cancer.DNA repair · 2019Review
- PARP-1 protects against colorectal tumor induction, but promotes inflammation-driven colorectal tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Trial watch - inhibiting PARP enzymes for anticancer therapy.Molecular & cellular oncology · 2016Review
- Genomic integration of lambda EG10 transgene in gpt delta transgenic rodents.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015Article
- Development of synthetic lethality anticancer therapeutics.Journal of medicinal chemistry · 2014Review
- PARP1 and DNA-PKcs synergize to suppress p53 mutation and telomere fusions during T-lineage lymphomagenesis.Oncogene · 2013Article
- Functional Aspects of PARP1 in DNA Repair and Transcription.Biomolecules · 2012Article
- Radiosensitization effect of poly(ADP-ribose) polymerase inhibition in cells exposed to low and high liner energy transfer radiation.Cancer science · 2012Article
- DNA base excision repair: a mechanism of trinucleotide repeat expansion.Trends in biochemical sciences · 2012Review
- Balancing repair and tolerance of DNA damage caused by alkylating agents.Nature reviews. Cancer · 2012Review
- Molecular and cellular pathways associated with chromosome 1p deletions during colon carcinogenesis.Clinical and experimental gastroenterology · 2011Article
- Mutational spectrum at GATA1 provides insights into mutagenesis and leukemogenesis in Down syndrome.Blood · 2009Article
- Genotoxic responses to titanium dioxide nanoparticles and fullerene in gpt delta transgenic MEF cells.Particle and fibre toxicology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulated evidence suggests that Parp-1 is involved in DNA repair processes, including base excision repair, single-strand and double-strand break repairs. To understand the precise role of Parp-1 in genomic stability in vivo, we carried out mutation analysis using Parp-1 knockout (Parp-1-/-) mice harboring two marker genes, gpt and red/gam genes. Spontaneous mutant frequencies of both genes in the bone marrows and livers did not differ significantly between Parp-1-/- and Parp-1+/+ mice (P>0.05). After treatment with an alkylating agent, N-nitrosobis(2-hydroxypropyl)amine (BHP), the mutant frequency of the red/gam genes in the liver in Parp-1-/- mice was 1.6-fold higher than that in Parp-1+/+ mice (P<0.05). Categorization of the mutations revealed that deletions larger than 1 kb or those accompanying 1-5 bp insertions at the deletion junctions, as well as rearrangements, were more frequently observed in Parp-1-/- than in Parp-1+/+ mice (P<0.05, respectively). In contrast, mutant frequencies of the gpt gene in the livers of Parp-1(-/-) and Parp-1(+/+) mice after BHP treatment were both elevated and there was no significant difference between the genotypes. These results indicate that Parp-1 is implicated in suppressing deletion mutations in vivo, especially those accompanying small insertions or rearrangements.
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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.