ArticleNature communications2014
Mechanistic insight into the interaction of BLM helicase with intra-strand G-quadruplex structures.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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.
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Who cites it
69 citing papers in PubMed, 97 citations in OpenAlex.
- Design, synthesis, and anti-prostate cancer activity evaluation of novel thieno[2,3-b]pyridine derivatives as potential BLM helicase inhibitors.Molecular diversity · 2026Article
- Canonical and noncanonical forms of G4 DNA at cluster III of the BCL6 breakpoint region could lead to chromosomal translocation in DLBCL.The Journal of biological chemistry · 2026Article
- Bloom syndrome helicase is required for efficient HIV-1 reverse transcription in macrophages.bioRxiv : the preprint server for biology · 2026Article
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Review
- A subcellular selective APEX2-based proximity labeling used for identifying mitochondrial G-quadruplex DNA binding proteins.Nucleic acids research · 2025Article
- Chemoproteomic profiling unveils binding and functional diversity of endogenous proteins that interact with endogenous triplex DNA.Nature chemistry · 2024Article
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Bioactive nutraceuticals as G4 stabilizers: potential cancer prevention and therapy-a critical review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Spotlight on G-Quadruplexes: From Structure and Modulation to Physiological and Pathological Roles.International journal of molecular sciences · 2024Review
- Structure, Topology, and Stability of Multiple G-quadruplexes in Long Telomeric Overhangs.Journal of molecular biology · 2024Review
- A CK2 and SUMO-dependent, PML NB-involved regulatory mechanism controlling BLM ubiquitination and G-quadruplex resolution.Nature communications · 2023Article
- BLM helicase protein negatively regulates stress granule formation through unwinding RNA G-quadruplex structures.Nucleic acids research · 2023Article
- In vivo dynamics and regulation of DNA G-quadruplex structures in mammals.Cell & bioscience · 2023Review
- Identification of G-quadruplex DNA sequences in SARS-CoV2.Immunogenetics · 2022Article
- Recognition and unfolding of human telomeric G-quadruplex by short peptide binding identified from the HRDC domain of BLM helicase.RSC advances · 2022Article
- G4-quadruplex-binding proteins: review and insights into selectivity.Biophysical reviews · 2022Review
- Bloom helicase mediates formation of large single-stranded DNA loops during DNA end processing.Nature communications · 2022Article
- RQC helical hairpin in Bloom's syndrome helicase regulates DNA unwinding by dynamically intercepting nascent nucleotides.iScience · 2022Article
9 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
9 authors at 5 institutions in 4 countries.
Funding
Abstract
Bloom syndrome is an autosomal recessive disorder caused by mutations in the RecQ family helicase BLM that is associated with growth retardation and predisposition to cancer. BLM helicase has a high specificity for non-canonical G-quadruplex (G4) DNA structures, which are formed by G-rich DNA strands and play an important role in the maintenance of genomic integrity. Here we used single-molecule FRET to define the mechanism of interaction of BLM helicase with intra-stranded G4 structures. We show that the activity of BLM is substrate dependent, and highly regulated by a short-strand DNA (ssDNA) segment that separates the G4 motif from double-stranded DNA. We demonstrate cooperativity between the RQC and HRDC domains of BLM during binding and unfolding of the G4 structure, where the RQC domain interaction with G4 is stabilized by HRDC binding to ssDNA. We present a model that proposes a unique role for G4 structures in modulating the activity of DNA processing enzymes.
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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.