ArticleNucleic acids research2019
The RecQ helicase Sgs1 drives ATP-dependent disruption of Rad51 filaments.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Synergistic effects of bloom helicase (BLM) inhibitor AO/854 with cisplatin in prostate cancer.Scientific reports · 2024Article
- All who wander are not lost: the search for homology during homologous recombination.Biochemical Society transactions · 2024Article
- Hi-C sequencing unravels dynamic three-dimensional chromatin interactions in muntjac lineage: insights from chromosome fusions in Fea's muntjac genome.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- A RAD51-ADP double filament structure unveils the mechanism of filament dynamics in homologous recombination.Nature communications · 2023Article
- Repair of DNA double-strand breaks in plant meiosis: role of eukaryotic RecA recombinases and their modulators.Plant reproduction · 2023Review
- Single Molecule Imaging of DNA-Protein Interactions Using DNA Curtains.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Discovery of a Novel Bloom's Syndrome Protein (BLM) Inhibitor Suppressing Growth and Metastasis of Prostate Cancer.International journal of molecular sciences · 2022Article
- Srs2 and Pif1 as Model Systems for Understanding Sf1a and Sf1b Helicase Structure and Function.Genes · 2021Review
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- Replication protein A plays multifaceted roles complementary to specialized helicases in processing G-quadruplex DNA.iScience · 2021Article
- The Bloom syndrome complex senses RPA-coated single-stranded DNA to restart stalled replication forks.Nature communications · 2021Article
- Single-molecule visualization of human RECQ5 interactions with single-stranded DNA recombination intermediates.Nucleic acids research · 2021Article
- Mechanistic Insights From Single-Molecule Studies of Repair of Double Strand Breaks.Frontiers in cell and developmental biology · 2021Review
- Development of a single-stranded DNA-binding protein fluorescent fusion toolbox.Nucleic acids research · 2020Article
- Review
- Review
- Review
- Review
- Rad52 Restrains Resection at DNA Double-Strand Break Ends in Yeast.Molecular cell · 2019Article
Corrections and comments
- Erratum issuedCorrection.2024
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
DNA helicases of the RecQ family are conserved among the three domains of life and play essential roles in genome maintenance. Mutations in several human RecQ helicases lead to diseases that are marked by cancer predisposition. The Saccharomyces cerevisiae RecQ helicase Sgs1 is orthologous to human BLM, defects in which cause the cancer-prone Bloom's Syndrome. Here, we use single-molecule imaging to provide a quantitative mechanistic understanding of Sgs1 activities on single stranded DNA (ssDNA), which is a central intermediate in all aspects of DNA metabolism. We show that Sgs1 acts upon ssDNA bound by either replication protein A (RPA) or the recombinase Rad51. Surprisingly, we find that Sgs1 utilizes a novel motor mechanism for disrupting ssDNA intermediates bound by the recombinase protein Rad51. The ability of Sgs1 to disrupt Rad51-ssDNA filaments may explain some of the defects engendered by RECQ helicase deficiencies in human cells.
Indexed as
Identifiers
What OpenQuestion holds
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.