ArticleNucleic acids research2026
Accessibility of telomeric overhangs to stabilizing small-molecule ligands.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
- Redox regulation of telomerase and telomeres in cancer: a critical appraisal of exposure, causality and molecular directness.Molecular biology reports · 2026Review
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9 authors.
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Abstract
Human chromosomes terminate in 50-300 nucleotide (nt) long single-stranded telomeric overhangs composed of repeating d(TTAGGG) sequences, which can fold into tandem G-quadruplex (GQ) structures protecting chromosome ends. Stabilizing GQs by small-molecules inhibits telomerase, motivating development of GQ-targeting anti-cancer agents. However, how interactions among successive GQs and bound ligands affect small-molecule accessibility remain unclear. We used single-molecule fluorescence microscopy and stepwise photobleaching to quantify binding stoichiometry of fluorescent oxazole telomestatin derivative L1Cy5-7OTD to telomeric overhangs capable of forming 1-6 GQs (30-162 nt long), spanning much of the physiologically relevant range. Longer overhangs bound more ligands on average but consistently below the theoretical maximum, saturating at six ligands even when 12 binding sites were available. Increasing the inter-GQ spacer from 3-nt to 9-nt enhanced ligand binding, a result independently confirmed by ensemble fluorescence enhancement experiments using N-methyl mesoporphyrin IX as a ligand. A one-dimensional lattice model, describing equilibrium ligand binding to partially ordered telomeric overhangs, revealed positive cooperativity between folding of successive GQs, negative cooperativity between ligands bound opposing (top and bottom) faces of successive GQs, and reduced affinity at duplex-single strand junction. These results show how telomeric architecture governs ligand accessibility and inform rational GQ-targeted drug design.
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