ArticleDNA repair2013
The RECQL4 protein, deficient in Rothmund-Thomson syndrome is active on telomeric D-loops containing DNA metabolism blocking lesions.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Selective interactions at pre-replication complexes categorize baseline and dormant origins.Nature communications · 2025Article
- Rothmund-Thomson syndrome, a disorder far from solved.Frontiers in aging · 2023Review
- Review
- Molecular Mechanisms of the RECQ4 Pathogenic Mutations.Frontiers in molecular biosciences · 2021Review
- Comprehensive Synthetic Genetic Array Analysis of Alleles That Interact with Mutation of theG3 (Bethesda, Md.) · 2020Article
- Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.Progress in biophysics and molecular biology · 2020Review
- Genetic analyses of aplastic anemia and idiopathic pulmonary fibrosis patients with short telomeres, possible implication of DNA-repair genes.Orphanet journal of rare diseases · 2019Article
- Subependymal giant cell astrocytoma-like astrocytoma: a neoplasm with a distinct phenotype and frequent neurofibromatosis type-1-association.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- TheThe Journal of biological chemistry · 2018Article
- Yeast Hrq1 shares structural and functional homology with the disease-linked human RecQ4 helicase.Nucleic acids research · 2017Article
- DNA-conjugated gold nanoparticles based colorimetric assay to assess helicase activity: a novel route to screen potential helicase inhibitors.Scientific reports · 2017Article
- Structural and biochemical characterization of an RNA/DNA binding motif in the N-terminal domain of RecQ4 helicases.Scientific reports · 2016Article
- The intrinsically disordered amino-terminal region of human RecQL4: multiple DNA-binding domains confer annealing, strand exchange and G4 DNA binding.Nucleic acids research · 2014Article
- Senescence induced by RECQL4 dysfunction contributes to Rothmund-Thomson syndrome features in mice.Cell death & disease · 2014Article
- Human RECQL1 participates in telomere maintenance.Nucleic acids research · 2014Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Telomeres are critical for cell survival and functional integrity. Oxidative DNA damage induces telomeric instability and cellular senescence that are associated with normal aging and segmental premature aging disorders such as Werner Syndrome and Rothmund-Thomson Syndrome, caused by mutations in WRN and RECQL4 helicases respectively. Characterizing the metabolic roles of RECQL4 and WRN in telomere maintenance is crucial in understanding the pathogenesis of their associated disorders. We have previously shown that WRN and RECQL4 display a preference in vitro to unwind telomeric DNA substrates containing the oxidative lesion 8-oxoguanine. Here, we show that RECQL4 helicase has a preferential activity in vitro on telomeric substrates containing thymine glycol, a critical lesion that blocks DNA metabolism, and can be modestly stimulated further on a D-loop structure by TRF2, a telomeric shelterin protein. Unlike that reported for telomeric D-loops containing 8-oxoguanine, RECQL4 does not cooperate with WRN to unwind telomeric D-loops with thymine glycol, suggesting RECQL4 helicase is selective for the type of oxidative lesion. RECQL4's function at the telomere is not yet understood, and our findings suggest a novel role for RECQL4 in the repair of thymine glycol lesions to promote efficient telomeric maintenance.
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