ArticleNature communications2023
UV-induced G4 DNA structures recruit ZRF1 which prevents UV-induced senescence.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 19 citations in OpenAlex.
- A Nutrient-Sensitive ZRF1-Dependent Secretory Network Involving S100A9 Contributes to Neutrophil Plasticity in Triple-Negative Breast Cancer.ACS pharmacology & translational science · 2026Article
- DNA damaging properties of G-quadruplex ligand QN-302 are potentiated by the DNA repair inhibitor Olaparib and mitigated by the molecular helicase PhpC.Genome biology · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Nuclear and Cytoplasmic Mouse ID Associated 1 (MIDA1) Protein Varies in Neurons and Astrocytes Across the Different Hippocampal Regions and Exhibits Age-Related Changes.Neurochemical research · 2026Article
- Stability of non-canonical nucleic acid structure as a potential modulator of cell fate.Nucleic acids research · 2026Review
- The Zuo1 C-terminal domain stabilizes DNA guanosine quadruplex (G4) structures located on Chromosome IX in Saccharomyces cerevisiae.Nucleic acids research · 2025Article
- Pharmacomodulation of G-quadruplexes in long non-coding RNAs dysregulated in colorectal cancer.BMC biology · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases.Nature reviews. Molecular cell biology · 2024Review
- Thermally Conductive and UV-EMI Shielding Electronic Textiles for Unrestricted and Multifaceted Health Monitoring.Nano-micro letters · 2024Article
- Selenomethionine in gelatin methacryloyl hydrogels: Modulating ferroptosis to attenuate skin aging.Bioactive materials · 2024Article
- G-quadruplex DNA and RNA in cellular senescence.Frontiers in aging · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence has two roles in oncology: it is known as a potent tumor-suppressive mechanism, which also supports tissue regeneration and repair, it is also known to contribute to reduced patient resilience, which might lead to cancer recurrence and resistance after therapy. Senescence can be activated in a DNA damage-dependent and -independent manner. It is not clear which type of genomic lesions induces senescence, but it is known that UV irradiation can activate cellular senescence in photoaged skin. Proteins that support the repair of DNA damage are linked to senescence but how they contribute to senescence after UV irradiation is still unknown. Here, we unraveled a mechanism showing that upon UV irradiation multiple G-quadruplex (G4) DNA structures accumulate in cell nuclei, which leads to the recruitment of ZRF1 to these G4 sites. ZRF1 binding to G4s ensures genome stability. The absence of ZRF1 triggers an accumulation of G4 structures, improper UV lesion repair, and entry into senescence. On the molecular level loss of ZRF1 as well as high G4 levels lead to the upregulation of DDB2, a protein associated with the UV-damage repair pathway, which drives cells into senescence.
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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 Socratic graph.