ArticleHuman molecular genetics2009
Direct and indirect roles of RECQL4 in modulating base excision repair capacity.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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.
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.
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Who cites it
55 citing papers in PubMed, 83 citations in OpenAlex.
- The Pathology of Viral Infections.Advances in experimental medicine and biology · 2026Review
- Review
- RECQL4 requires PARP1 for recruitment to DNA damage, and PARG dePARylation facilitates its associated role in end joining.Experimental & molecular medicine · 2025Article
- Rothmund-Thomson syndrome, a disorder far from solved.Frontiers in aging · 2023Review
- RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1.The Journal of clinical investigation · 2022Article
- Human Variation in DNA Repair, Immune Function, and Cancer Risk.Frontiers in immunology · 2022Review
- Review
- Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction.The Journal of investigative dermatology · 2021Review
- RECQL4 regulates DNA damage response and redox homeostasis in esophageal cancer.Cancer biology & medicine · 2021Article
- Clinical challenges in interpreting multiple pathogenic mutations in single patients.Hereditary cancer in clinical practice · 2021Article
- Molecular Mechanisms of the RECQ4 Pathogenic Mutations.Frontiers in molecular biosciences · 2021Review
- Human RecQ Helicases in DNA Double-Strand Break Repair.Frontiers in cell and developmental biology · 2021Review
- Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase.Nucleic acids research · 2020Article
- ATP-dependent helicase activity is dispensable for the physiological functions of Recql4.PLoS genetics · 2019Article
- Rothmund-Thomson Syndrome: Insights from New Patients on the Genetic Variability Underpinning Clinical Presentation and Cancer Outcome.International journal of molecular sciences · 2018Article
- Upregulation of RECQL4 expression predicts poor prognosis in hepatocellular carcinoma.Oncology letters · 2018Article
- Fanconi anaemia and cancer: an intricate relationship.Nature reviews. Cancer · 2018Review
- Osteosarcoma: Molecular Pathogenesis and iPSC Modeling.Trends in molecular medicine · 2017Review
- Control of structure-specific endonucleases to maintain genome stability.Nature reviews. Molecular cell biology · 2017Review
- Ribosomal Protein S3 Negatively Regulates Unwinding Activity of RecQ-like Helicase 4 through Their Physical Interaction.The Journal of biological chemistry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
RECQL4 is a human RecQ helicase which is mutated in approximately two-thirds of individuals with Rothmund-Thomson syndrome (RTS), a disease characterized at the cellular level by chromosomal instability. BLM and WRN are also human RecQ helicases, which are mutated in Bloom and Werner's syndrome, respectively, and associated with chromosomal instability as well as premature aging. Here we show that primary RTS and RECQL4 siRNA knockdown human fibroblasts accumulate more H(2)O(2)-induced DNA strand breaks than control cells, suggesting that RECQL4 may stimulate repair of H(2)O(2)-induced DNA damage. RTS primary fibroblasts also accumulate more XRCC1 foci than control cells in response to endogenous or induced oxidative stress and have a high basal level of endogenous formamidopyrimidines. In cells treated with H(2)O(2), RECQL4 co-localizes with APE1, and FEN1, key participants in base excision repair. Biochemical experiments indicate that RECQL4 specifically stimulates the apurinic endonuclease activity of APE1, the DNA strand displacement activity of DNA polymerase beta, and incision of a 1- or 10-nucleotide flap DNA substrate by Flap Endonuclease I. Additionally, RTS cells display an upregulation of BER pathway genes and fail to respond like normal cells to oxidative stress. The data herein support a model in which RECQL4 regulates both directly and indirectly base excision repair capacity.
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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.