ArticleNucleic acids research2010
Altered gene expression in the Werner and Bloom syndromes is associated with sequences having G-quadruplex forming potential.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 158 citations in OpenAlex.
- Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription.Oncogene · 2026Article
- 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
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Loss of DHX36/G4R1, a G4 resolvase, drives genome instability and regulates innate immune gene expression in cancer cells.Nucleic acids research · 2025Article
- Article
- Dynamic Structures and Fast Transition Kinetics of Oxidized G-Quadruplexes.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Base pair dynamics, electrostatics, and thermodynamics at the LTR-III quadruplex:duplex junction.Biophysical journal · 2024Article
- Spotlight on G-Quadruplexes: From Structure and Modulation to Physiological and Pathological Roles.International journal of molecular sciences · 2024Review
- Genomic Instability of G-Quadruplex Sequences inGenes · 2023Article
- Discovery of a new hereditary RECQ helicase disorder RECON syndrome positions the replication stress response and genome homeostasis as centrally important processes in aging and age-related disease.Ageing research reviews · 2023Review
- G-quadruplexes and associated proteins in aging and Alzheimer's disease.Frontiers in aging · 2023Review
- Targeting G-quadruplex for rescuing impaired chondrogenesis in WRN-deficient stem cells.Cell & bioscience · 2022Article
- Article
- Creation and resolution of non-B-DNA structural impediments during replication.Critical reviews in biochemistry and molecular biology · 2022Article
- Transcriptional regulation by a RecQ helicase.Methods in enzymology · 2022Article
- Chemical targeting of G-quadruplexes in telomeres and beyond for molecular cancer therapeutics.The Journal of antibiotics · 2021Review
- Cation competition and recruitment around the c-kit1 G-quadruplex using polarizable simulations.Biophysical journal · 2021Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The human Werner and Bloom syndromes (WS and BS) are caused by deficiencies in the WRN and BLM RecQ helicases, respectively. WRN, BLM and their Saccharomyces cerevisiae homologue Sgs1, are particularly active in vitro in unwinding G-quadruplex DNA (G4-DNA), a family of non-canonical nucleic acid structures formed by certain G-rich sequences. Recently, mRNA levels from loci containing potential G-quadruplex-forming sequences (PQS) were found to be preferentially altered in sgs1Delta mutants, suggesting that G4-DNA targeting by Sgs1 directly affects gene expression. Here, we extend these findings to human cells. Using microarrays to measure mRNAs obtained from human fibroblasts deficient for various RecQ family helicases, we observe significant associations between loci that are upregulated in WS or BS cells and loci that have PQS. No such PQS associations were observed for control expression datasets, however. Furthermore, upregulated genes in WS and BS showed no or dramatically reduced associations with sequences similar to PQS but that have considerably reduced potential to form intramolecular G4-DNA. These findings indicate that, like Sgs1, WRN and BLM can regulate transcription globally by targeting G4-DNA.
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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.