ArticleCell death & disease2014
Senescence induced by RECQL4 dysfunction contributes to Rothmund-Thomson syndrome features in mice.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- Isoswitching drives the aging process in human brains.bioRxiv : the preprint server for biology · 2025Article
- Review
- Unraveling the mechanisms of RECQL4-mediated cervical cancer progression through the PI3K/AKT pathway.Translational oncology · 2024Article
- Review
- Autophagy Dysfunction: The Kernel of Hair Loss?Clinical, cosmetic and investigational dermatology · 2024Review
- G-quadruplex DNA and RNA in cellular senescence.Frontiers in aging · 2024Review
- RecQ dysfunction contributes to social and depressive-like behavior and affects aldolase activity in mice.Neurobiology of disease · 2023Article
- De novo myelodysplastic syndrome in a Rothmund-Thomson Syndrome patient with novel pathogenicBlood science (Baltimore, Md.) · 2023Article
- Understanding the Impact of Obesity on Ageing in the Radiance of DNA Metabolism.The journal of nutrition, health & aging · 2023Review
- Article
- DNA-PKcs-dependent phosphorylation of RECQL4 promotes NHEJ by stabilizing the NHEJ machinery at DNA double-strand breaks.Nucleic acids research · 2022Article
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- RecQ-like helicase 4 (RECQL4) exacerbates resistance to oxaliplatin in colon adenocarcinoma via activation of the PI3K/AKT signaling pathway.Bioengineered · 2021Article
- Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction.The Journal of investigative dermatology · 2021Review
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- RECQL4 regulates DNA damage response and redox homeostasis in esophageal cancer.Cancer biology & medicine · 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
- Aberrantly Expressed RECQL4 Helicase Supports Proliferation and Drug Resistance of Human Glioma Cells and Glioma Stem Cells.Cancers · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence refers to irreversible growth arrest of primary eukaryotic cells, a process thought to contribute to aging-related degeneration and disease. Deficiency of RecQ helicase RECQL4 leads to Rothmund-Thomson syndrome (RTS), and we have investigated whether senescence is involved using cellular approaches and a mouse model. We first systematically investigated whether depletion of RECQL4 and the other four human RecQ helicases, BLM, WRN, RECQL1 and RECQL5, impacts the proliferative potential of human primary fibroblasts. BLM-, WRN- and RECQL4-depleted cells display increased staining of senescence-associated β-galactosidase (SA-β-gal), higher expression of p16(INK4a) or/and p21(WAF1) and accumulated persistent DNA damage foci. These features were less frequent in RECQL1- and RECQL5-depleted cells. We have mapped the region in RECQL4 that prevents cellular senescence to its N-terminal region and helicase domain. We further investigated senescence features in an RTS mouse model, Recql4-deficient mice (Recql4(HD)). Tail fibroblasts from Recql4(HD) showed increased SA-β-gal staining and increased DNA damage foci. We also identified sparser tail hair and fewer blood cells in Recql4(HD) mice accompanied with increased senescence in tail hair follicles and in bone marrow cells. In conclusion, dysfunction of RECQL4 increases DNA damage and triggers premature senescence in both human and mouse cells, which may contribute to symptoms in RTS patients.
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