ArticlePloS one2012
Hyperactivation of PARP triggers nonhomologous end-joining in repair-deficient mouse fibroblasts.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 33 citations in OpenAlex.
- Parkinson's disease linked LRRK2 G2019S drives oxidative nuclear DNA damage and PARP1 hyperactive signaling.bioRxiv : the preprint server for biology · 2026Article
- Short-term consumption of the modified standard American diet perturbed the metabolic balance and altered DNA damage in MMTV-PyMT transgenic mice.Breast cancer research : BCR · 2025Article
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
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- Poly (ADP-ribose) Interacts With Phosphorylated α-Synuclein in Post Mortem PD Samples.Frontiers in aging neuroscience · 2021Article
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- Defective base excision repair in the response to DNA damaging agents in triple negative breast cancer.PloS one · 2019Article
- XRCC1 phosphorylation affects aprataxin recruitment and DNA deadenylation activity.DNA repair · 2018Article
- DNA polymerase β: A missing link of the base excision repair machinery in mammalian mitochondria.DNA repair · 2017Article
- XRCC1-mediated repair of strand breaks independent of PNKP binding.DNA repair · 2017Article
- Application of Laser Micro-irradiation for Examination of Single and Double Strand Break Repair in Mammalian Cells.Journal of visualized experiments : JoVE · 2017Article
- Role of the oxidized form of XRCC1 in protection against extreme oxidative stress.Free radical biology & medicine · 2017Article
- DNA polymerase β contains a functional nuclear localization signal at its N-terminus.Nucleic acids research · 2017Article
- Micro-irradiation tools to visualize base excision repair and single-strand break repair.DNA repair · 2015Review
- Article
- Bisphenol a promotes cell survival following oxidative DNA damage in mouse fibroblasts.PloS one · 2015Article
- The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction.Nature communications · 2014Article
- Base excision repair defects invoke hypersensitivity to PARP inhibition.Molecular cancer research : MCR · 2014Article
- Suicidal cross-linking of PARP-1 to AP site intermediates in cells undergoing base excision repair.Nucleic acids research · 2014Article
- TNF-induced necroptosis and PARP-1-mediated necrosis represent distinct routes to programmed necrotic cell death.Cellular and molecular life sciences : CMLS · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Regulation of poly(ADP-ribose) (PAR) synthesis and turnover is critical to determining cell fate after genotoxic stress. Hyperactivation of PAR synthesis by poly(ADP-ribose) polymerase-1 (PARP-1) occurs when cells deficient in DNA repair are exposed to genotoxic agents; however, the function of this hyperactivation has not been adequately explained. Here, we examine PAR synthesis in mouse fibroblasts deficient in the base excision repair enzyme DNA polymerase β (pol β). The extent and duration of PARP-1 activation was measured after exposure to either the DNA alkylating agent, methyl methanesulfonate (MMS), or to low energy laser-induced DNA damage. There was strong DNA damage-induced hyperactivation of PARP-1 in pol β nullcells, but not in wild-type cells. In the case of MMS treatment, PAR synthesis did not lead to cell death in the pol β null cells, but instead resulted in increased PARylation of the nonhomologous end-joining (NHEJ) protein Ku70 and increased association of Ku70 with PARP-1. Inhibition of the NHEJ factor DNA-PK, under conditions of MMS-induced PARP-1 hyperactivation, enhanced necrotic cell death. These data suggest that PARP-1 hyperactivation is a protective mechanism triggering the classical-NHEJ DNA repair pathway when the primary alkylated base damage repair pathway is compromised.
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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.