ArticleOncogene2000
Differential regulation of human RecQ family helicases in cell transformation and cell cycle.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 123 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
- Prognostic Significance of DNA Repair Gene mRNA Expression in Early-Stage Breast Cancer: Insights into Clinical Relevance.Oncology research · 2026Article
- Pan-Cancer Analysis of WRN: From Multi-Omics Biomarker Discovery to Therapy-Guiding Functional Evidence.OncoTargets and therapy · 2026Article
- Specific Monitoring the DNA Helicase Function via Anchor-Embedded DNA Probe.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Resistance to DNA repair inhibitors in cancer.Molecular oncology · 2022Review
- RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022Review
- WRN helicase safeguards deprotected replication forks in BRCA2-mutated cancer cells.Nature communications · 2021Article
- Article
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- RecQL4-Aurora B kinase axis is essential for cellular proliferation, cell cycle progression, and mitotic integrity.Oncogenesis · 2018Article
- Distinct prognosis of mRNA expression of the five RecQ DNA-helicase family members -Cancer management and research · 2018Article
- RECQ1 expression is upregulated in response to DNA damage and in a p53-dependent manner.Oncotarget · 2017Article
- Mechanistic and biological considerations of oxidatively damaged DNA for helicase-dependent pathways of nucleic acid metabolism.Free radical biology & medicine · 2017Review
- Insights into the RecQ helicase mechanism revealed by the structure of the helicase domain of human RECQL5.Nucleic acids research · 2017Article
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.Molecular syndromology · 2017Review
- Recombine and Associate to Prevent Genomic Instability and Premature Aging.Molecular syndromology · 2017Article
- WRN Promoter CpG Island Hypermethylation Does Not Predict More Favorable Outcomes for Patients with Metastatic Colorectal Cancer Treated with Irinotecan-Based Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Catalytic strand separation by RECQ1 is required for RPA-mediated response to replication stress.Current biology : CB · 2015Article
5 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
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Three human RecQ DNA helicases, WRN, BLM and RTS, are involved in the genetic disorders associated with genomic instability and a high incidence of cancer. RecQL1 and RecQL5 also belong to the human RecQ helicase family, but their correlation with genetic disorders, if any, is unknown. We report here that in human B cells transformed by Epstein-Barr virus (EBV), human fibroblasts and umbilical endothelial cells transformed by simian virus 40, the expression of WRN, BLM, RTS and RecQL1 was sharply up-regulated. In B cells this expression was stimulated within 5-40 h by the tumor promoting agent phorbol myristic acetate (PMA). Interestingly, RecQL5beta, an alternative splicing product of RecQL5 with a nuclear localization signal, is expressed in resting B cells without significant modulation of its synthesis by EBV or PMA, suggesting it has a role in resting cells. We also roughly determined the number of copies per cell for the five RecQ helicase in B cells. In addition, levels of the different RecQ helicases are modulated in different ways during the cell cycle of actively proliferating fibroblasts and umbilical endothelial cells. Our results support the view that the levels of WRN, BLM, RTS and RecQL1 are differentially up-regulated to guarantee genomic stability in cells that are transformed or actively proliferating.
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.