ArticleNucleic acids research2014
Suicidal cross-linking of PARP-1 to AP site intermediates in cells undergoing base excision repair.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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.
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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
58 citing papers in PubMed, 90 citations in OpenAlex.
- Fork Reversal Safeguards Epigenetic Inheritance During Replication Stress.Research square · 2026Article
- DNA-Protein Cross-Links Derived from Abasic DNA Lesions: Recent Progress and Future Directions.Chemical research in toxicology · 2025Review
- CHD6 has poly(ADP-ribose)- and DNA-binding domains and regulates PARP1/2-trapping inhibitor sensitivity via abasic site repair.Nature communications · 2025Article
- The human Shu complex promotes RAD51 activity by modulating RPA dynamics on ssDNA.Nature communications · 2024Article
- Isolation and detection of DNA-protein crosslinks in mammalian cells.Nucleic acids research · 2024Article
- Enzymatic Processing of DNA-Protein Crosslinks.Genes · 2024Review
- Temporal recruitment of base excision DNA repair factors in living cells in response to different micro-irradiation DNA damage protocols.DNA repair · 2023Article
- APE1 promotes non-homologous end joining by initiating DNA double-strand break formation and decreasing ubiquitination of artemis following oxidative genotoxic stress.Journal of translational medicine · 2023Article
- Hallmarks of DNA replication stress.Molecular cell · 2022Review
- XRCC1 counteracts poly(ADP ribose)polymerase (PARP) poisons, olaparib and talazoparib, and a clinical alkylating agent, temozolomide, by promoting the removal of trapped PARP1 from broken DNA.Genes to cells : devoted to molecular & cellular mechanisms · 2022Article
- Human TDP1, APE1 and TREX1 repair 3'-DNA-peptide/protein cross-links arising from abasic sites in vitro.Nucleic acids research · 2022Article
- Article
- Targeting DNA-Protein CrosslinksFrontiers in molecular biosciences · 2022Review
- Replication-dependent cytotoxicity and Spartan-mediated repair of trapped PARP1-DNA complexes.Nucleic acids research · 2021Article
- Topoisomerase Assays.Current protocols · 2021Article
- DNA polymerases η and κ bypass NThe Journal of biological chemistry · 2021Article
- Translesion activity of PrimPol on DNA with cisplatin and DNA-protein cross-links.Scientific reports · 2021Article
- XRCC1 prevents toxic PARP1 trapping during DNA base excision repair.Molecular cell · 2021Article
- When DNA Polymerases Multitask: Functions Beyond Nucleotidyl Transfer.Frontiers in molecular biosciences · 2021Review
- Treatment of human cells with 5-aza-dC induces formation of PARP1-DNA covalent adducts at genomic regions targeted by DNMT1.DNA repair · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant nuclear enzyme in mammalian cells. The enzyme synthesizes polymers of ADP-ribose from the coenzyme NAD(+) and plays multifaceted roles in cellular responses to genotoxic stress, including DNA repair. It had been shown that mouse fibroblasts treated with a DNA methylating agent in combination with a PARP inhibitor exhibit higher cytotoxicity than cells treated with methylating agent alone. This lethality of the PARP inhibitor is dependent on apurinic/apyrimidinic (AP) sites in the DNA and the presence of PARP-1. Here, we show that purified PARP-1 is capable of forming a DNA-protein cross-link (DPC) by covalently attaching to the AP site. This DPC formation is specific to the presence of the natural AP site in DNA and is accompanied by a single-strand DNA incision. Cellular studies confirm the formation of PARP-1 DPCs during alkylating agent-induced base excision repair (BER) and formation of DPCs is enhanced by a PARP inhibitor. Using an N-terminal and C-terminal truncated PARP-1 we show that a polypeptide fragment comprising the zinc 3 and BRCT sub-domains is sufficient for DPC formation. The covalent attachment of PARP-1 to AP site-containing DNA appears to be a suicidal event when BER is overwhelmed or disrupted.
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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.