ArticleBMC cell biology2003
Poly(ADP-ribose) polymerase (PARP-1) is not involved in DNA double-strand break recovery.
Article in BMC cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Efficacy and safety of veliparib plus chemotherapy for the treatment of lung cancer: A systematic review of clinical trials.PloS one · 2023Pooled it
- Poly(ADP-ribose) polymerase inhibition: past, present and future.Nature reviews. Drug discovery · 2020Review
- Tailoring Ovarian Cancer Treatment: Implications ofCancers · 2019Review
- PARP-2 depletion results in lower radiation cell survival but cell line-specific differences in poly(ADP-ribose) levels.Cellular and molecular life sciences : CMLS · 2015Article
- Induction of homologous recombination following in utero exposure to DNA-damaging agents.DNA repair · 2013Article
- Radiosensitization in prostate cancer: mechanisms and targets.BMC urology · 2013Review
- Repair of DNA strand breaks in a minichromosome in vivo: kinetics, modeling, and effects of inhibitors.PloS one · 2013Article
- Extract of Lillium candidum L. can modulate the genotoxicity of the antibiotic zeocin.Molecules (Basel, Switzerland) · 2011Article
- Targeting poly(ADP-ribose) polymerase activity for cancer therapy.Cellular and molecular life sciences : CMLS · 2010Review
- Prostate cancer radiosensitization through poly(ADP-Ribose) polymerase-1 hyperactivation.Cancer research · 2010Article
- Making the best of PARP inhibitors in ovarian cancer.Nature reviews. Clinical oncology · 2010Review
- Sensitization to radiation and alkylating agents by inhibitors of poly(ADP-ribose) polymerase is enhanced in cells deficient in DNA double-strand break repair.Molecular cancer therapeutics · 2010Article
- PARP inhibition versus PARP-1 silencing: different outcomes in terms of single-strand break repair and radiation susceptibility.Nucleic acids research · 2008Article
- Induction of DNA double-strand breaks by zeocin in Chlamydomonas reinhardtii and the role of increased DNA double-strand breaks rejoining in the formation of an adaptive response.Radiation and environmental biophysics · 2007Article
- Parp-1 protects homologous recombination from interference by Ku and Ligase IV in vertebrate cells.The EMBO journal · 2006Article
- PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways.Nucleic acids research · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe cytotoxicity and the rejoining of DNA double-strand breaks induced by gamma-rays, H2O2 and neocarzinostatin, were investigated in normal and PARP-1 knockout mouse 3T3 fibroblasts to determine the role of poly(ADP-ribose) polymerase (PARP-1) in DNA double-strand break repair.
resultsPARP-1-/- were considerably more sensitive than PARP-1+/+ 3T3s to induced cell kill by gamma-rays and H2O2. However, the two cell lines did not show any significant difference in the susceptibility to neocarzinostatin below 1.5 nM drug. Restoration of PARP-1 expression in PARP-1-/- 3T3s by retroviral transfection of the full PARP-1 cDNA did not induce any change in neocarzinostatin response. Moreover the incidence and the rejoining kinetics of neocarzinostatin-induced DNA double-strand breaks were identical in PARP-1+/+ and PARP-1-/- 3T3s. Poly(ADP-ribose) synthesis following gamma-rays and H2O2 was observed in PARP-1-proficient cells only. In contrast neocarzinostatin, even at supra-lethal concentration, was unable to initiate PARP-1 activation yet it induced H2AX histone phosphorylation in both PARP1+/+ and PARP-1-/- 3T3s as efficiently as gamma-rays and H2O2.
conclusionsThe results show that PARP-1 is not a major determinant of DNA double-strand break recovery with either strand break rejoining or cell survival as an endpoint. Even though both PARP-1 and ATM activation are major determinants of the cell response to gamma-rays and H2O2, data suggest that PARP-1-dependent poly(ADP-ribose) synthesis and ATM-dependent H2AX phosphorylation, are not inter-related in the repair pathway of neocarzinostatin-induced DNA double-strand breaks.
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