ArticleCell cycle (Georgetown, Tex.)2011
Transcription-induced DNA toxicity at trinucleotide repeats: double bubble is trouble.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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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
32 citing papers in PubMed, 38 citations in OpenAlex.
- Unstable FGF14 GAA repeat expansions in Indian ataxia patients: a broader phenotype and involvement of modifier loci?Journal of human genetics · 2025Article
- CAG Repeat Instability and Region-Specific Gene Expression Changes in the SCA12 Brain.Cerebellum (London, England) · 2025Article
- DNA Mismatch Repair and its Role in Huntington's Disease.Journal of Huntington's disease · 2021Review
- R-loops promote trinucleotide repeat deletion through DNA base excision repair enzymatic activities.The Journal of biological chemistry · 2020Article
- New Roles for Canonical Transcription Factors in Repeat Expansion Diseases.Trends in genetics : TIG · 2020Review
- The role of fork stalling and DNA structures in causing chromosome fragility.Genes, chromosomes & cancer · 2019Review
- R-loop generation during transcription: Formation, processing and cellular outcomes.DNA repair · 2018Review
- Structure and Dynamics of DNA and RNA Double Helices Obtained from the CCG and GGC Trinucleotide Repeats.The journal of physical chemistry. B · 2018Article
- A novel mode for transcription inhibition mediated by PNA-induced R-loops with a model in vitro system.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
- E-motif formed by extrahelical cytosine bases in DNA homoduplexes of trinucleotide and hexanucleotide repeats.Nucleic acids research · 2018Article
- Strong transcription blockage mediated by R-loop formation within a G-rich homopurine-homopyrimidine sequence localized in the vicinity of the promoter.Nucleic acids research · 2017Article
- Translocation and deletion breakpoints in cancer genomes are associated with potential non-B DNA-forming sequences.Nucleic acids research · 2016Article
- Mismatch repair enhances convergent transcription-induced cell death at trinucleotide repeats by activating ATR.DNA repair · 2016Article
- Fanconi anemia pathway regulates convergent transcription-induced cell death at trinucleotide repeats in human cells.Postdoc journal : a journal of postdoctoral research and postdoctoral affairs · 2016Article
- PNA binding to the non-template DNA strand interferes with transcription, suggesting a blockage mechanism mediated by R-loop formation.Molecular carcinogenesis · 2015Article
- Twisting right to left: A…A mismatch in a CAG trinucleotide repeat overexpansion provokes left-handed Z-DNA conformation.PLoS computational biology · 2015Article
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Coupling transcriptional state to large-scale repeat expansions in yeast.Cell reports · 2014Article
- A genome-wide map of adeno-associated virus-mediated human gene targeting.Nature structural & molecular biology · 2014Article
- RNA-protein interactions in unstable microsatellite diseases.Brain research · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Trinucleotide repeats (TNR) are a blessing and a curse. In coding regions, where they are enriched, short repeats offer the potential for continuous, rapid length variation with linked incremental changes in the activity of the encoded protein, a valuable source of variation for evolution. But at the upper end of these benign and beneficial lengths, trinucleotide repeats become very unstable, with a dangerous bias toward continual expansion, which can lead to neurological diseases in humans. The mechanisms of expansion are varied and the links to disease are complex. Where they have been delineated, however, they have often revealed unexpected, fundamental aspects of the underlying cell biology. Nowhere is this more apparent than in recent studies, which indicate that expanded CAG repeats can form toxic sites in the genome, which can, upon interaction with normal components of DNA metabolism, trigger cell death. Here we discuss the phenomenon of TNR-induced DNA toxicity, with special emphasis on the role of transcription. Transcription-induced DNA toxicity may have profound biological consequences, with particular relevance to repeat-associated neurodegenerative diseases.
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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.