ArticleNucleic acids research2014
PARP3 affects the relative contribution of homologous recombination and nonhomologous end-joining pathways.
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 72 papers.
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Who cites it
72 citing papers in PubMed, 96 citations in OpenAlex.
- Structural basis of PARP2 recognition of nucleosomal DNA breaks and inhibitor trapping.Nucleic acids research · 2026Article
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- Post-translational modification networks in tumor radiosensitivity: mechanistic insights and therapeutic opportunities.Journal of translational medicine · 2026Review
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Future of PARP inhibitors in cancer treatment: overcoming resistance and enhancing efficacy with combination therapies.Journal of Zhejiang University. Science. B · 2025Review
- Review
- Amphiphilic Oligonucleotide Derivatives as a Tool to Study DNA Repair Proteins.International journal of molecular sciences · 2025Article
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- PARP Inhibitors in Ovarian Cancer: Resistance Mechanisms, Clinical Evidence, and Evolving Strategies.Biomedicines · 2025Review
- Parp3 assists muscle function and skeletal muscle differentiation by selectively adjusting H3K27me3 enrichment.iScience · 2025Article
- PARP4 deficiency enhances sensitivity to ATM inhibitor by impairing DNA damage repair in melanoma.Cell death discovery · 2025Article
- Mono-ADP-ribosylation, a MARylationmultifaced modification of protein, DNA and RNA: characterizations, functions and mechanisms.Cell death discovery · 2024Review
- Review
- Gene expression of non-homologous end-joining pathways in the prognosis of ovarian cancer.iScience · 2023Article
- Review
- Review
- Article
- PARP3 supervises G9a-mediated repression of adhesion and hypoxia-responsive genes in glioblastoma cells.Scientific reports · 2022Article
- The expanding universe of PARP1-mediated molecular and therapeutic mechanisms.Molecular cell · 2022Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
Abstract
The repair of toxic double-strand breaks (DSB) is critical for the maintenance of genome integrity. The major mechanisms that cope with DSB are: homologous recombination (HR) and classical or alternative nonhomologous end joining (C-NHEJ versus A-EJ). Because these pathways compete for the repair of DSB, the choice of the appropriate repair pathway is pivotal. Among the mechanisms that influence this choice, deoxyribonucleic acid (DNA) end resection plays a critical role by driving cells to HR, while accurate C-NHEJ is suppressed. Furthermore, end resection promotes error-prone A-EJ. Increasing evidence define Poly(ADP-ribose) polymerase 3 (PARP3, also known as ARTD3) as an important player in cellular response to DSB. In this work, we reveal a specific feature of PARP3 that together with Ku80 limits DNA end resection and thereby helps in making the choice between HR and NHEJ pathways. PARP3 interacts with and PARylates Ku70/Ku80. The depletion of PARP3 impairs the recruitment of YFP-Ku80 to laser-induced DNA damage sites and induces an imbalance between BRCA1 and 53BP1. Both events result in compromised accurate C-NHEJ and a concomitant increase in DNA end resection. Nevertheless, HR is significantly reduced upon PARP3 silencing while the enhanced end resection causes mutagenic deletions during A-EJ. As a result, the absence of PARP3 confers hypersensitivity to anti-tumoral drugs generating DSB.
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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.