ArticleMolecular and cellular biology2005
Recql5 and Blm RecQ DNA helicases have nonredundant roles in suppressing crossovers.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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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
80 citing papers in PubMed, 121 citations in OpenAlex.
- Bloom syndrome helicase is required for efficient HIV-1 reverse transcription in macrophages.bioRxiv : the preprint server for biology · 2026Article
- Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.Nucleic acids research · 2025Article
- Structural basis of RECQL5-induced RNA polymerase II transcription braking and subsequent reactivation.Nature structural & molecular biology · 2025Article
- A Recql5 mutant facilitates complex CRISPR/Cas9-mediated chromosomal engineering in mouse zygotes.Genetics · 2024Article
- FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress.Nature communications · 2024Article
- Review
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- Bromodomain proteins: protectors against endogenous DNA damage and facilitators of genome integrity.Experimental & molecular medicine · 2021Review
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- ATRX and RECQ5 define distinct homologous recombination subpathways.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- TRIM28 functions as the SUMO E3 ligase for PCNA in prevention of transcription induced DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- RECQL5 at theFrontiers in cell and developmental biology · 2020Review
- RECQL5 plays an essential role in maintaining genome stability and viability of triple-negative breast cancer cells.Cancer medicine · 2019Article
- Putting together and taking apart: assembly and disassembly of the Rad51 nucleoprotein filament in DNA repair and genome stability.Cell stress · 2018Review
- BLM helicase regulates DNA repair by counteracting RAD51 loading at DNA double-strand break sites.The Journal of cell biology · 2017Article
- Article
- Clinicopathological and prognostic significance of RECQL5 helicase expression in breast cancers.Carcinogenesis · 2016Article
- RECQ helicases are deregulated in hematological malignancies in association with a prognostic value.Biomarker research · 2016Article
- Recql5 protects against lipopolysaccharide/D-galactosamine-induced liver injury in mice.World journal of gastroenterology · 2015Article
20 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
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotes, crossovers in mitotic cells can have deleterious consequences and therefore must be suppressed. Mutations in BLM give rise to Bloom syndrome, a disease that is characterized by an elevated rate of crossovers and increased cancer susceptibility. However, simple eukaryotes such as Saccharomyces cerevisiae have multiple pathways for suppressing crossovers, suggesting that mammals also have multiple pathways for controlling crossovers in their mitotic cells. We show here that in mouse embryonic stem (ES) cells, mutations in either the Bloom syndrome homologue (Blm) or the Recql5 genes result in a significant increase in the frequency of sister chromatid exchange (SCE), whereas deleting both Blm and Recql5 lead to an even higher frequency of SCE. These data indicate that Blm and Recql5 have nonredundant roles in suppressing crossovers in mouse ES cells. Furthermore, we show that mouse embryonic fibroblasts derived from Recql5 knockout mice also exhibit a significantly increased frequency of SCE compared with the corresponding wild-type control. Thus, this study identifies a previously unknown Recql5-dependent, Blm-independent pathway for suppressing crossovers during mitosis in mice.
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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.