ArticleNature communications2025
ssG4-seq for global profiling of strand-specific G-quadruplex structures in mammalian genomes.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- Direct visualisation of post-replication gap formation at the bacterial RRS.bioRxiv : the preprint server for biology · 2026Article
- Modulating G-quadruplexes for therapeutic intervention: Structural diversity, stability, and emerging nucleic-acid-based strategies.Molecular therapy. Nucleic acids · 2026Review
- Identification of G4-regulated immune-related drug targets for prostate cancer based on G4 screen and machine learning.Frontiers in immunology · 2026Article
- ssG4-seq for global profiling of strand-specific G-quadruplex structures in mammalian genomes.Nature communications · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
DNA G-quadruplexes (G4s), formed by guanine-rich sequences in mammalian genomes, are non-canonical structures implicated in gene regulation. However, their strand-specific genomic distribution and mechanistic roles in transcription remain poorly understood. Here, we report a strand-specific G4 sequencing (ssG4-seq) method for global profiling of G4 structures across multiple mammalian genomes. This method faithfully recapitulates known G4 structures and identifies thousands of previously unannotated G4s in human K562 cells. Remarkably, over 95% of G4s are located at enhancers and promoters across species, with promoters containing dual-strand G4s exhibiting significantly stronger transcriptional activation compared to those with single-strand G4s. Mechanistically, we identify SP1 as a potent G4 reader that facilitates transcription by modulating enhancer-promoter chromatin looping. Furthermore, we demonstrate that cancer-associated mutations can destabilize G4 structures, impair SP1-mediated chromatin interactions, and contribute to tumorigenesis. Our study demonstrates the power of ssG4-seq in elucidating G4 functions in gene regulation and disease.
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Registered trials
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