ArticleProceedings of the National Academy of Sciences of the United States of America1995
A dominant-negative mutant of human poly(ADP-ribose) polymerase affects cell recovery, apoptosis, and sister chromatid exchange following DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 203 citations in OpenAlex.
- Depletion of Zinc Causes Osteoblast Apoptosis with Elevation of Leptin Secretion and Phosphorylation of JAK2/STAT3.Nutrients · 2022Article
- Pharmacologic Induction of BRCAness inCancers · 2022Review
- Poly(ADP-Ribose)Polymerase (PARP) Inhibitors and Radiation Therapy.Frontiers in pharmacology · 2020Review
- PARP Inhibitors in Prostate Cancer—The Preclinical Rationale and Current Clinical Development.Genes · 2019Review
- Antitumor effect of kurarinone and underlying mechanism in small cell lung carcinoma cells.OncoTargets and therapy · 2019Article
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
- Synthetic viability by BRCA2 and PARP1/ARTD1 deficiencies.Nature communications · 2016Article
- LRP1 Regulates Retinal Angiogenesis by Inhibiting PARP-1 Activity and Endothelial Cell Proliferation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- The efficiency of Poly(ADP-Ribose) Polymerase (PARP) cleavage on detection of apoptosis in an experimental model of testicular torsion.International journal of experimental pathology · 2015Article
- let-7b suppresses apoptosis and autophagy of human mesenchymal stem cells transplanted into ischemia/reperfusion injured heart 7by targeting caspase-3.Stem cell research & therapy · 2015Article
- Response of Dictyostelium discoideum to UV-C and involvement of poly (ADP-ribose) polymerase.Cell proliferation · 2015Article
- Role of PARP-1 in prostate cancer.American journal of clinical and experimental urology · 2015Review
- Poly(ADP-ribose) polymerase-1 causes mitochondrial damage and neuron death mediated by Bnip3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- ARTD1 (PARP1) activation and NAD(+) in DNA repair and cell death.DNA repair · 2014Review
- Poly(ADP-ribose) polymerase-1 and its cleavage products differentially modulate cellular protection through NF-kappaB-dependent signaling.Biochimica et biophysica acta · 2014Article
- Review of poly (ADP-ribose) polymerase (PARP) mechanisms of action and rationale for targeting in cancer and other diseases.Critical reviews in eukaryotic gene expression · 2014Review
- Crosstalk between poly(ADP-ribose) polymerase and sirtuin enzymes.Molecular aspects of medicine · 2013Review
- Involvement of homologous recombination in the synergism between cisplatin and poly (ADP-ribose) polymerase inhibition.Cancer science · 2013Article
- Enhanced killing of cancer cells by poly(ADP-ribose) polymerase inhibitors and topoisomerase I inhibitors reflects poisoning of both enzymes.The Journal of biological chemistry · 2012Article
- Novel role for the transient receptor potential channel TRPM2 in prostate cancer cell proliferation.Prostate cancer and prostatic diseases · 2010Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase [PARP; NAD+ ADP-ribosyltransferase; NAD+:poly(adenosine-diphosphate-D-ribosyl)-acceptor ADP-D-ribosyltransferase, EC 2.4.2.30] is a zinc-dependent eukaryotic DNA-binding protein that specifically recognizes DNA strand breaks produced by various genotoxic agents. To study the biological function of this enzyme, we have established stable HeLa cell lines that constitutively produce the 46-kDa DNA-binding domain of human PARP (PARP-DBD), leading to the trans-dominant inhibition of resident PARP activity. As a control, a cell line was constructed, producing a point-mutated version of the DBD, which has no affinity for DNA in vitro. Expression of the PARP-DBD had only a slight effect on undamaged cells but had drastic consequences for cells treated with genotoxic agents. Exposure of cell lines expressing the wild-type (wt) or the mutated PARP-DBD, with low doses of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resulted in an increase in their doubling time, a G2 + M accumulation, and a marked reduction in cell survival. However, UVC irradiation had no preferential effect on the cell growth or viability of cell lines expressing the PARP-DBD. These PARP-DBD-expressing cells treated with MNNG presented the characteristic nucleosomal DNA ladder, one of the hallmarks of cell death by apoptosis. Moreover, these cells exhibited chromosomal instability as demonstrated by higher frequencies of both spontaneous and MNNG-induced sister chromatid exchanges. Surprisingly, the line producing the mutated DBD had the same behavior as those producing the wt DBD, indicating that the mechanism of action of the dominant-negative mutant involves more than its DNA-binding function. Altogether, these results strongly suggest that PARP is an element of the G2 checkpoint in mammalian cells.
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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.