ArticleNature communications2020
Mechanisms of telomerase inhibition by oxidized and therapeutic dNTPs.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 56 citations in OpenAlex.
- γ-Glutamylcysteine alleviates hypertension and vascular remodeling in SHR by suppressing oxidative stress through Keap1 S-glutathionylation.Redox report : communications in free radical research · 2026Article
- Manganese Dioxide Nanoparticles Protect PC12 Cells Against HPharmaceutics · 2026Article
- Design, synthesis, anticancer activity and molecular modeling of new pyrazoline derivatives as telomerase inhibitors.RSC advances · 2026Article
- Therapeutic 6-thio-deoxyguanosine inhibits telomere elongation in cancer cells by inducing a non-productive stalled telomerase complex.Nature communications · 2025Article
- Cell-selective telomere damage by thiopurine-based oligonucleotide for diffuse large B cell lymphoma immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Identification and Characterization of Glycine- and Proline-Rich Antioxidant Peptides From Antler Residues Based on Peptidomics, Machine Learning, and Molecular Docking.Food science & nutrition · 2025Article
- High-Throughput Screening Tool to Identify Small Molecule Inhibitors of Telomerase.ACS chemical biology · 2025Article
- Development of a microarray based telomerase binding assay reveals unusual binding of a cytochalasin derivative.Scientific reports · 2025Article
- Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025Review
- Human Brain Organoids: Development and Applications.Journal of microbiology and biotechnology · 2025Review
- Canonical and non-canonical functions of the non-coding RNA component (TERC) of telomerase complex.Cell & bioscience · 2025Review
- HACE1 as a bridge between oxidative stress and autophagy.Frontiers in immunology · 2025Review
- Role of MTH1 in oxidative stress and therapeutic targeting of cancer.Redox biology · 2024Review
- The 8-oxoguanine DNA glycosylase-synaptotagmin 7 pathway increases extracellular vesicle release and promotes tumour metastasis during oxidative stress.Journal of extracellular vesicles · 2024Article
- Chiral coordination polymer nanowires boost radiation-induced in situ tumor vaccination.Nature communications · 2024Article
- Article
- Mitochondria and telomeres: hand in glove.Biogerontology · 2024Review
- Reduced SIRT1 and SIRT3 and Lower Antioxidant Capacity of Seminal Plasma Is Associated with Shorter Sperm Telomere Length in Oligospermic Men.International journal of molecular sciences · 2024Article
- New insights into methods to measure biological age: a literature review.Frontiers in aging · 2024Review
- Leukocyte telomere length and lung function: a mendelian randomization study in European population.Frontiers in physiology · 2024Article
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 2 institutions in 1 country.
Funding
Abstract
Telomerase is a specialized reverse transcriptase that adds GGTTAG repeats to chromosome ends and is upregulated in most human cancers to enable limitless proliferation. Here, we uncover two distinct mechanisms by which naturally occurring oxidized dNTPs and therapeutic dNTPs inhibit telomerase-mediated telomere elongation. We conduct a series of direct telomerase extension assays in the presence of modified dNTPs on various telomeric substrates. We provide direct evidence that telomerase can add the nucleotide reverse transcriptase inhibitors ddITP and AZT-TP to the telomeric end, causing chain termination. In contrast, telomerase continues elongation after inserting oxidized 2-OH-dATP or therapeutic 6-thio-dGTP, but insertion disrupts translocation and inhibits further repeat addition. Kinetics reveal that telomerase poorly selects against 6-thio-dGTP, inserting with similar catalytic efficiency as dGTP. Furthermore, telomerase processivity factor POT1-TPP1 fails to restore processive elongation in the presence of inhibitory dNTPs. These findings reveal mechanisms for targeting telomerase with modified dNTPs in cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.