ArticleDNA and cell biology2015
Novel cytoprotective inhibitors for apoptotic endonuclease G.
Article in DNA and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Discovery of an Endonuclease G-inhibitory Ku80-peptide protecting against leukemogenic rearrangements at the MLL breakpoint cluster.Nature communications · 2026Article
- Nuclear endonuclease G controls cell proliferation in ovarian cancer.FEBS open bio · 2023Article
- Article
- Duck Tembusu virus infection induces mitochondrial-mediated and death receptor-mediated apoptosis in duck embryo fibroblasts.Veterinary research · 2022Article
- Biallelic Variants inCells · 2022Article
- Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response.Nature communications · 2021Article
- A Fibrinogen Alpha Fragment Mitigates Chemotherapy-InducedFrontiers in oncology · 2021Article
- The Dual Regulation of Apoptosis by Flavivirus.Frontiers in microbiology · 2021Review
- Mitochondrial Dysfunction and Multiple Sclerosis.Biology · 2019Review
- Histone deacetylase inhibitors protect against cisplatin-induced acute kidney injury by activating autophagy in proximal tubular cells.Cell death & disease · 2018Article
- Mechanism of graphene-induced cytotoxicity: Role of endonucleases.Journal of applied toxicology : JAT · 2017Article
- Melittin induces human gastric cancer cell apoptosis via activation of mitochondrial pathway.World journal of gastroenterology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptotic endonuclease G (EndoG) is responsible for DNA fragmentation both during and after cell death. Previous studies demonstrated that genetic inactivation of EndoG is cytoprotective against various pro-apoptotic stimuli; however, specific inhibitors for EndoG are not available. In this study, we have developed a high-throughput screening assay for EndoG and have used it to screen a chemical library. The screening resulted in the identification of two potent EndoG inhibitors, PNR-3-80 and PNR-3-82, which are thiobarbiturate analogs. As determined by their IC₅₀s, the inhibitors are more potent than ZnCl₂ or EDTA. They inhibit EndoG at one or two orders of magnitude greater than another apoptotic endonuclease, DNase I, and do not inhibit the other five tested cell death-related enzymes: DNase II, RNase A, proteinase, lactate dehydrogenase, and superoxide dismutase 1. Exposure of natural EndoG-expressing 22Rv1 or EndoG-overexpressing PC3 cells rendered them significantly resistant to Cisplatin and Docetaxel, respectively. These novel EndoG inhibitors have the potential to be utilized for amelioration of cell injuries in which participation of EndoG is essential.
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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.