ArticleNucleic acids research2000
Base excision repair is efficient in cells lacking poly(ADP-ribose) polymerase 1.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 127 citations in OpenAlex.
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Roles of ADP-Ribosyltransferases in Cancer.Oncology research · 2026Review
- Effective Radiosensitization of HNSCC Cell Lines by DNA-PKcs Inhibitor AZD7648 and PARP Inhibitors Talazoparib and Niraparib.International journal of molecular sciences · 2024Article
- PARP1 Gene Knockout Suppresses Expression of DNA Base Excision Repair Genes.Doklady. Biochemistry and biophysics · 2023Article
- Review
- PARP Inhibitor Resistance Mechanisms and Implications for Post-Progression Combination Therapies.Cancers · 2020Review
- PARP Inhibitors: Clinical Relevance, Mechanisms of Action and Tumor Resistance.Frontiers in cell and developmental biology · 2020Review
- PARP inhibition and immune modulation: scientific rationale and perspectives for the treatment of gynecologic cancers.Therapeutic advances in medical oncology · 2020Review
- MacroH2A1 Regulation of Poly(ADP-Ribose) Synthesis and Stability Prevents Necrosis and Promotes DNA Repair.Molecular and cellular biology · 2019Article
- Cytoplasmic PARP-1 promotes pancreatic cancer tumorigenesis and resistance.International journal of cancer · 2019Article
- ERCC1-deficient cells and mice are hypersensitive to lipid peroxidation.Free radical biology & medicine · 2018Article
- Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.British journal of pharmacology · 2018Review
- Kinetics of poly(ADP-ribosyl)ation, but not PARP1 itself, determines the cell fate in response to DNA damage in vitro and in vivo.Nucleic acids research · 2017Article
- Olaparib modulates DNA repair efficiency, sensitizes cervical cancer cells to cisplatin and exhibits anti-metastatic property.Scientific reports · 2017Article
- The multifaceted roles of PARP1 in DNA repair and chromatin remodelling.Nature reviews. Molecular cell biology · 2017Review
- Poly(adenosine diphosphate-ribose) polymerase as therapeutic target: lessons learned from its inhibitors.Oncotarget · 2017Review
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
- Beet root juice protects against doxorubicin toxicity in cardiomyocytes while enhancing apoptosis in breast cancer cells.Molecular and cellular biochemistry · 2016Article
- The XRCC1 phosphate-binding pocket binds poly (ADP-ribose) and is required for XRCC1 function.Nucleic acids research · 2015Article
- Regulation of NEIL1 protein abundance by RAD9 is important for efficient base excision repair.Nucleic acids research · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that is activated by binding to DNA breaks induced by ionizing radiation or through repair of altered bases in DNA by base excision repair. Mice lacking PARP-1 and, in certain cases, the cells derived from these mice exhibit hypersensitivity to ionizing radiation and alkylating agents. In this study we investigated base excision repair in cells lacking PARP-1 in order to elucidate whether their augmented sensitivity to DNA damaging agents is due to an impairment of the base excision repair pathway. Extracts prepared from wild-type cells or cells lacking PARP-1 were similar in their ability to repair plasmid DNA damaged by either X-rays (single-strand DNA breaks) or by N:-methyl-N:'-nitro-N:-nitrosoguanidine (methylated bases). In addition, we demonstrated in vivo that PARP-1-deficient cells treated with N:-methyl-N:'-nitro-N:-nitrosoguanidine repaired their genomic DNA as efficiently as wild-type cells. Therefore, we conclude that cells lacking PARP-1 have a normal capacity to repair single-strand DNA breaks inflicted by X-irradiation or breaks formed during the repair of modified bases. We propose that the hypersensitivity of PARP-1 null mutant cells to gamma-irradiation and alkylating agents is not directly due to a defect in DNA repair itself, but rather results from greatly reduced poly(ADP-ribose) formation during base excision repair in these cells.
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