ArticleCancer genomics & proteomics
Duplex DNA from Sites of Helicase-Polymerase Uncoupling Links Non-B DNA Structure Formation to Replicative Stress.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The Influence of CG sites on dynamic DNA sequence mutagenesis in the genomic evolution of mammalian lifespan.Nucleic acids research · 2025Article
- Twisting tetraplex DNA: A strand dynamics regulating i-motif function in diverse molecular crowding environments.Nucleic acids research · 2025Article
- Chromatin Immunoprecipitation Reveals p53 Binding to G-Quadruplex DNA Sequences in Myeloid Leukemia Cell Lines.ACS bio & med chem Au · 2025Article
- Stabilization of expandable DNA repeats by the replication factor Mcm10 promotes cell viability.Nature communications · 2024Article
- Replication-induced DNA secondary structures drive fork uncoupling and breakage.The EMBO journal · 2023Article
- i-Motif formation and spontaneous deletions in human cells.Nucleic acids research · 2022Article
- Remodeling the conformational dynamics of I-motif DNA by helicases in ATP-independent mode at acidic environment.iScience · 2022Article
- The potential interplay between G-quadruplex and p53: their roles in regulation of ferroptosis in cancer.Frontiers in molecular biosciences · 2022Review
- Genomic Frequencies of Dynamic DNA Sequences and Mammalian Lifespan.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundReplication impediments can produce helicase-polymerase uncoupling allowing lagging strand synthesis to continue for as much as 6 kb from the site of the impediment. MATERIALS AND
methodsWe developed a cloning procedure designed to recover fragments from lagging strand near the helicase halt site.
resultsA total of 62% of clones from a p53-deficient tumor cell line (PC3) and 33% of the clones from a primary cell line (HPS-19I) were within 5 kb of a G-quadruplex forming sequence. Analyses of a RACK7 gene sequence, that was cloned multiple times from the PC3 line, revealed multiple deletions in region about 1 kb from the cloned region that was present in a non-B conformation. Sequences from the region formed G-quadruplex and i-motif structures under physiological conditions.
conclusionDefects in components of non-B structure suppression systems (e.g. p53 helicase targeting) promote replication-linked damage selectively targeted to sequences prone to G-quadruplex and i-motif formation.
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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.