ArticleNature communications2018
BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genes.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 115 citations in OpenAlex.
- Article
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
- A small molecule disrupts G4-STAT1 interaction and synergizes with olaparib to drive cancer cell death.Nucleic acids research · 2026Article
- Strand-seq and the future of personalized genomics.Nature genetics · 2026Review
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- G-quadruplexes regulate chromatin accessibility and gene expression in Bloom Syndrome.bioRxiv : the preprint server for biology · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- Indirect identification of genomic G-quadruplexes via a small protein probe that specifically recognizes C-rich single-stranded DNA.Nucleic acids research · 2026Article
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- HLTF cooperates with GATA1 to activate transcriptional programs and chromatin remodeling during erythroid development.Nucleic acids research · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Review
- Review
- Review
- Copy number normalization distinguishes differential signals driven by copy number differences in ATAC-seq and ChIP-seq.BMC genomics · 2025Article
- Article
- YY1 is involved in homologous recombination inhibition at guanine quadruplex sites in human cells.Nucleic acids research · 2024Article
- Circ_0001671 regulates prostate cancer progression through miR-27b-3p/BLM axis.Scientific reports · 2024Article
- Spotlight on G-Quadruplexes: From Structure and Modulation to Physiological and Pathological Roles.International journal of molecular sciences · 2024Review
19 more citing papers are in PubMed but not listed here.
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
Bloom syndrome is a cancer predisposition disorder caused by mutations in the BLM helicase gene. Cells from persons with Bloom syndrome exhibit striking genomic instability characterized by excessive sister chromatid exchange events (SCEs). We applied single-cell DNA template strand sequencing (Strand-seq) to map the genomic locations of SCEs. Our results show that in the absence of BLM, SCEs in human and murine cells do not occur randomly throughout the genome but are strikingly enriched at coding regions, specifically at sites of guanine quadruplex (G4) motifs in transcribed genes. We propose that BLM protects against genome instability by suppressing recombination at sites of G4 structures, particularly in transcribed regions of the genome.
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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.