ReviewCommunications biology2026
Rare genetic diseases associated with G-quadruplex-induced replication stress.
Review in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Cryo-EM structures of human FANCJ reveal the mechanism of G-quadruplex unwinding and disease-associated mutations.Nature communications · 2026Article
- SARS-CoV-2 Nsp13 helicase resolves G-quadruplexes and is inhibited by G4 ligands or an antiviral regulator: Implications for G4 anti-coronavirus therapies.The Journal of biological chemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replication stress is incurred by endogenous or environmental challenges to replication fork progression that impede faithful genome duplication. Genomic G-quadruplexes (G4s) are DNA secondary structures that present a substantial barrier for passage of the replisome, and DNA synthesis past these structures requires dynamic remodeling by specialized helicases, translocases, and other G4-binding proteins to facilitate G4 resolution or bypass. Mutations in the genes encoding these auxiliary replication proteins are linked to hereditary disorders presenting with a range of clinical features, including immunodeficiency, growth restriction, congenital abnormalities, and cancer predisposition, demonstrating that these G4-metabolizing proteins also play broader roles in genome biology such as the replication stress response or DNA repair. Here, we review rare diseases linked to mutations in G4-resolving and binding proteins, with an emphasis on molecular defects in G4 metabolism that incur replication stress and genomic instability. We discuss differences in G4 substrate specificity and mechanism of G4-interactive helicases, as revealed by high-resolution structural data. Furthermore, we address outstanding questions that provide insight into the etiology of rare diseases marked by dysregulated G4 homeostasis and may inform diagnosis and potential therapeutic strategies.
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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 Socratic graph.