ArticleMolecular and cellular biology2007
RECQL, a member of the RecQ family of DNA helicases, suppresses chromosomal instability.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 108 citations in OpenAlex.
- RECQ1 A159C Polymorphism Is Associated With Overall Survival of Patients With Resected Pancreatic Cancer: A Replication Study in NRG Oncology Radiation Therapy Oncology Group 9704.International journal of radiation oncology, biology, physics · 2016Trial
- A transcription factor regulates development of a bacteria-housing eukaryotic cell through DNA damage mitigation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- RecQ dysfunction contributes to social and depressive-like behavior and affects aldolase activity in mice.Neurobiology of disease · 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
- Case report: Germline RECQL mutation potentially involved in hereditary predisposition to acute leukemia.Frontiers in oncology · 2023Article
- Genome-wide investigations on regulatory functions of RECQ1 helicase.Methods (San Diego, Calif.) · 2022Article
- RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1.The Journal of clinical investigation · 2022Article
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- Transcriptional regulation by a RecQ helicase.Methods in enzymology · 2022Article
- High Expression of RECQL Protein in ER-Positive Breast Tumours Is Associated With a Better Survival.Frontiers in oncology · 2022Article
- ID3 promotes homologous recombination via non-transcriptional and transcriptional mechanisms and its loss confers sensitivity to PARP inhibition.Nucleic acids research · 2021Article
- Genome-Wide Analysis Unveils DNA Helicase RECQ1 as a Regulator of Estrogen Response Pathway in Breast Cancer Cells.Molecular and cellular biology · 2021Article
- Human RecQ Helicases in DNA Double-Strand Break Repair.Frontiers in cell and developmental biology · 2021Review
- RECQ1 Helicase in Genomic Stability and Cancer.Genes · 2020Review
- Replication Fork Remodeling and Therapy Escape in DNA Damage Response-Deficient Cancers.Frontiers in oncology · 2020Review
- The DNA repair helicase RECQ1 has a checkpoint-dependent role in mediating DNA damage responses induced by gemcitabine.The Journal of biological chemistry · 2019Article
- Clinical implications of germline mutations in breast cancer genes: RECQL.Breast cancer research and treatment · 2019Review
- Transcriptome profiling of coriander: a dual purpose crop unravels stem gall resistance genes.Journal of genetics · 2019Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 4 countries.
Funding
Abstract
The mouse gene Recql is a member of the RecQ subfamily of DEx-H-containing DNA helicases. Five members of this family have been identified in both humans and mice, and mutations in three of these, BLM, WRN, and RECQL4, are associated with human diseases and a cellular phenotype that includes genomic instability. To date, no human disease has been associated with mutations in RECQL and no cellular phenotype has been associated with its deficiency. To gain insight into the physiological function of RECQL, we disrupted Recql in mice. RECQL-deficient mice did not exhibit any apparent phenotypic differences compared to wild-type mice. Cytogenetic analyses of embryonic fibroblasts from the RECQL-deficient mice revealed aneuploidy, spontaneous chromosomal breakage, and frequent translocation events. In addition, the RECQL-deficient cells were hypersensitive to ionizing radiation, exhibited an increased load of DNA damage, and displayed elevated spontaneous sister chromatid exchanges. These results provide evidence that RECQL has a unique cellular role in the DNA repair processes required for genomic integrity. Genetic background, functional redundancy, and perhaps other factors may protect the unstressed mouse from the types of abnormalities that might be expected from the severe chromosomal aberrations detected at the cellular level.
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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 OpenQuestion graph.