ArticleOncogene2004
Effects of novel inhibitors of poly(ADP-ribose) polymerase-1 and the DNA-dependent protein kinase on enzyme activities and DNA repair.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 108 citations in OpenAlex.
- Emergence of Nanotechnology as a Powerful Cavalry against Triple-Negative Breast Cancer (TNBC).Pharmaceuticals (Basel, Switzerland) · 2022Review
- Article
- The molecular basis and disease relevance of non-homologous DNA end joining.Nature reviews. Molecular cell biology · 2020Review
- Chemical Decorations of "MARs" Residents in Orchestrating Eukaryotic Gene Regulation.Frontiers in cell and developmental biology · 2020Review
- EGFR Mutations Compromise Hypoxia-Associated Radiation Resistance through Impaired Replication Fork-Associated DNA Damage Repair.Molecular cancer research : MCR · 2017Article
- DNA repair kinetics in SCID mice Sertoli cells and DNA-PKcs-deficient mouse embryonic fibroblasts.Chromosoma · 2017Article
- Assessment of PARP protein expression in epithelial ovarian cancer by ELISA pharmacodynamic assay and immunohistochemistry.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Therapeutic targets of triple-negative breast cancer: a review.British journal of pharmacology · 2015Review
- TNKS1BP1 functions in DNA double-strand break repair though facilitating DNA-PKcs autophosphorylation dependent on PARP-1.Oncotarget · 2015Article
- Article
- DNA ligase III acts as a DNA strand break sensor in the cellular orchestration of DNA strand break repair.Nucleic acids research · 2015Article
- Review
- PARP1 and DNA-PKcs synergize to suppress p53 mutation and telomere fusions during T-lineage lymphomagenesis.Oncogene · 2013Article
- Repair of DNA strand breaks in a minichromosome in vivo: kinetics, modeling, and effects of inhibitors.PloS one · 2013Article
- Zinc Finger Nuclease induced DNA double stranded breaks and rearrangements in MLL.Mutation research · 2012Article
- Role of DNA-dependent protein kinase catalytic subunit in cancer development and treatment.Translational cancer research · 2012Article
- Visualization of a DNA-PK/PARP1 complex.Nucleic acids research · 2012Article
- Regulation of chromatin structure by poly(ADP-ribosyl)ation.Frontiers in genetics · 2012Article
- Hyperactivation of PARP triggers nonhomologous end-joining in repair-deficient mouse fibroblasts.PloS one · 2012Article
- Poly(ADP-ribose) polymerase inhibition enhances p53-dependent and -independent DNA damage responses induced by DNA damaging agent.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA-dependent protein kinase (DNA-PK) and poly (ADP-ribose) polymerase-1 (PARP-1) participate in nonhomologous end joining and base excision repair, respectively, and are key determinants of radio- and chemo-resistance. Both PARP-1 and DNA-PK have been identified as therapeutic targets for anticancer drug development. Here we investigate the effects of specific inhibitors on enzyme activities and DNA double-strand break (DSB) repair. The enzyme activities were investigated using purified enzymes and in permeabilized cells. Inhibition, or loss of activity, was compared using potent inhibitors of DNA-PK (NU7026) and PARP-1 (AG14361), and cell lines proficient or deficient for DNA-PK or PARP-1. Inactive DNA-PK suppressed the activity of PARP-1 and vice versa. This was not the consequence of simple substrate competition, since DNA ends were provided in excess. The inhibitory effect of DNA-PK on PARP activity was confirmed in permeabilized cells. Both inhibitors prevented ionizing radiation-induced DSB repair, but only AG14361 prevented single-strand break repair. An increase in DSB levels caused by inhibition of PARP-1 was shown to be caused by a decrease in DSB repair, and not by the formation of additional DSBs. These data point to combined inhibition of PARP-1 and DNA-PK as a powerful strategy for tumor radiosensitization.
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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.